A functional food with effects of improving insomnia and anxiety

Abstract

The application discloses a functional food with effects of improving insomnia and anxiety, and each raw material is composed of ganoderma extract 5-12 parts, salvia miltiorrhiza extract 5-15 parts, astragalus extract 5-15 parts, jujube extract 3-15 parts, anemarrhena asphodeloides extract 3-12 parts and cyperus rotundus extract 2-10 parts; each raw material is a solid powder of water extract. The application aims to overcome the defects of traditional sedative and tranquilizing drugs and dietary supplement methods, and make up for the defects of the lack of functional food for effectively and simultaneously regulating neural homeostasis and improving insomnia and anxiety symptoms in the market. The functional food can regulate neurotransmitter balance, inhibit the oxidation and inflammation level of the body, effectively improve sleep disorders and relieve anxiety, and improve the sleep quality and emotional homeostasis of the body.

Description

Technical Field

[0001] This invention relates to the field of functional food technology, and in particular to a functional food that can improve both insomnia and anxiety. Background Technology

[0002] Long-term mental stress, emotional imbalance, and other factors can disrupt the body's neurotransmitter secretion, breaking the balance between excitation and inhibition in the central nervous system, leading to insomnia problems such as difficulty falling asleep, sleep maintenance disorders, and early awakening. Insomnia and anxiety can easily form a vicious cycle: long-term insomnia can further cause hyperfunction of the hypothalamus-pituitary-adrenal axis, prompting the release of large amounts of inflammatory factors and the accumulation of oxidative stress products, inducing persistent anxiety, which in turn exacerbates sleep disorders. The long-term coexistence of these two factors not only damages sleep quality and emotional state but also significantly increases the risk of chronic diseases such as hypertension, diabetes, and obesity. Therefore, how to gently regulate central nervous system homeostasis, improve insomnia, and alleviate anxiety, thereby fundamentally breaking the vicious cycle of mutual aggravation, is a core issue of common concern for people with insomnia, functional food R&D companies, and clinical medical researchers.

[0003] Currently, the mainstream clinical interventions for insomnia accompanied by anxiety mainly employ chemical sedatives and tranquilizers such as benzodiazepines, non-benzodiazepine hypnotics, and 5-HT reuptake inhibitors. While these drugs can quickly suppress central nervous system excitation, shorten sleep onset time, and alleviate severe anxiety symptoms, long-term use can easily lead to adverse reactions such as dizziness, drowsiness, daytime fatigue, and memory loss. They also carry the risks of drug dependence and withdrawal rebound, providing only short-term symptomatic intervention and failing to fundamentally regulate the body's neurotransmitter secretion and endocrine homeostasis. Furthermore, existing dietary supplements have single targets, only slightly improving difficulty falling asleep and failing to simultaneously alleviate the anxiety associated with insomnia, resulting in long treatment cycles and weak overall intervention effects. Currently, there is a lack of multifunctional foods on the market that can simultaneously improve insomnia, relieve anxiety, regulate neurological homeostasis, and reduce the body's inflammation levels. Therefore, developing functional foods suitable for people with chronic insomnia and anxiety is of significant practical importance for improving sleep quality, regulating mood, and enhancing daily mental vitality. Summary of the Invention

[0004] To address the aforementioned problems in existing technologies, this invention provides a functional food that can improve insomnia and alleviate anxiety. This invention aims to overcome the shortcomings of traditional sedative and tranquilizing drugs and dietary supplements, while simultaneously filling the gap in the market for functional foods that effectively regulate neurological homeostasis and improve insomnia accompanied by anxiety symptoms. This functional food can regulate neurotransmitter balance, inhibit oxidative inflammation levels in the body, effectively improve sleep disorders, alleviate anxiety, and enhance sleep quality and emotional homeostasis.

[0005] The technical solution of the present invention is as follows: The first objective of this invention is to provide a functional food that improves both insomnia and anxiety, wherein the ingredients, by weight, are composed of: 5-12 parts of Ganoderma lucidum extract 5-15 parts of tanshinone extract 5-15 parts of Astragalus extract Jujube extract 3-15 parts Anemarrhena asphodeloides extract 3-12 parts Cyperus rotundus extract 2-10 parts; All raw materials are solid powders derived from water extracts.

[0006] In one embodiment of the present invention, the ingredients of the functional food are composed of the following components by weight: 5.8 parts of Ganoderma lucidum extract 5.3 parts of tanshinone extract Astragalus extract 5.0 parts Jujube extract 3.3 parts Anemarrhena asphodeloides extract 3.3 parts Cyperus rotundus extract 2.5 parts.

[0007] In one embodiment of the present invention, the content of Ganoderma lucidum polysaccharides in the Ganoderma lucidum extract is ≥10%, and the content of total triterpenes and sterols is ≥5%.

[0008] In one embodiment of the present invention, the content of tanshinone IIA in the tanshinone extract is ≥1.0%.

[0009] In one embodiment of the present invention, the content of astragaloside IV in the Astragalus extract is ≥0.5%.

[0010] In one embodiment of the present invention, the content of jujube polysaccharide in the jujube extract is ≥15%.

[0011] In one embodiment of the present invention, the content of anemarrhena saponin BⅡ in the anemarrhena extract is ≥8%.

[0012] In one embodiment of the present invention, the content of α-cyperone in the Cyperus rotundus extract is ≥1.0%.

[0013] In one embodiment of the present invention, the content of the active ingredient in each extract is a mass percentage.

[0014] In one embodiment of the present invention, the dosage form of the functional food is granules, tablets, capsules, powders, granules, or tea bags.

[0015] In one embodiment of the present invention, the functional food includes health food.

[0016] In one embodiment of the invention, the functional food also includes food-acceptable excipients.

[0017] In one embodiment of the present invention, the excipients of the functional food include maltodextrin and steviol glycosides.

[0018] The second objective of this invention is to provide an application of the above-mentioned functional food for preparing health foods that have the effects of improving insomnia and anxiety.

[0019] A third objective of this invention is to provide a method for preparing the above-mentioned functional food, wherein the functional food is in granule form, comprising the following steps: (1) Mix 5-12 parts of Ganoderma lucidum extract, 5-15 parts of Salvia miltiorrhiza extract, 5-15 parts of Astragalus membranaceus extract, 3-15 parts of jujube extract, 3-12 parts of Anemarrhena asphodeloides extract and 2-10 parts of Cyperus rotundus extract evenly to obtain a raw material mixture. (2) Add 0-10 parts of maltodextrin and 0-0.2 parts of steviol glycosides to the raw material mixture and mix thoroughly to obtain a soft material; (3) The soft material is granulated, dried and sized at a temperature below 60°C to obtain the granule product.

[0020] A fourth objective of this invention is to provide a method for preparing the above-mentioned functional food, wherein the functional food is a capsule, comprising the following steps: (1) Mix 5-12 parts of Ganoderma lucidum extract, 5-15 parts of Salvia miltiorrhiza extract, 5-15 parts of Astragalus membranaceus extract, 3-15 parts of jujube extract, 3-12 parts of Anemarrhena asphodeloides extract and 2-10 parts of Cyperus rotundus extract evenly to obtain a raw material mixture. (2) Place the raw material mixture together with 0-10 parts of maltodextrin and 0-0.2 parts of steviol glycosides in a mixer and pulverize and mix thoroughly to obtain a uniform dry powder mixture; (3) The dry powder mixture is filled into a capsule shell to obtain the capsule product.

[0021] In one embodiment of the present invention, the effect of improving insomnia with anxiety includes balancing central neurotransmitters, inhibiting oxidative inflammation in the body, reducing sleep latency, increasing sleep duration, relieving anxiety, and stabilizing the body's sleep and emotional homeostasis.

[0022] In one embodiment of the present invention, improving insomnia accompanied by anxiety symptoms in an animal model includes: alleviating weight loss in mice, reducing sleep latency in mice, increasing sleep duration in mice, increasing the distance mice can cross the central grid in an open field experiment, increasing the time, number of times and total distance mice can enter the open arm in an elevated cross maze experiment, reducing the anxiety index in mice, improving pathological damage to the hippocampus in mice, upregulating GABA and 5-HT levels in the hippocampus of mice, downregulating DA and NE levels in the hippocampus of mice, downregulating serum pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) levels, and upregulating serum anti-inflammatory cytokines (IL-10) levels.

[0023] In one embodiment of the present invention, improving the pathological characteristics of patients with insomnia and anxiety in clinical treatment includes: reducing the Pittsburgh Sleep Quality Index (PSQI) score, reducing the Insomnia Severity Index (ISI) score, reducing the Epworth Sleepiness Scale (ESS) score, reducing the Generalized Anxiety Scale (GAD-7) score, and reducing the Self-Rating Depression Scale (PHQ-9) score.

[0024] Beneficial effects: This invention follows the theory of traditional Chinese medicine compatibility and integrates modern neuromodulation mechanisms. It can safely and effectively improve insomnia and relieve anxiety by synergistically regulating neurotransmitter levels and inhibiting the body's oxidative inflammatory response through multiple pathways.

[0025] This invention has verified through animal experiments that a functional food composed of Ganoderma lucidum extract, Salvia miltiorrhiza extract, Astragalus membranaceus extract, jujube extract, Anemarrhena asphodeloides extract, and Cyperus rotundus extract has the effect of relieving insomnia accompanied by anxiety, specifically manifested in: (1) It helps mice with insomnia and anxiety to recover their weight; (2) Decrease and increase the sleep latency and sleep duration in mice with insomnia and anxiety, respectively; (3) Increase the distance that insomnia-associated anxiety mice can travel across the central grid in the open field experiment; (4) Increase the time, number of times and total distance for mice with insomnia and anxiety to enter the open arm in the elevated cross maze experiment, and reduce the anxiety index of the mice; (5) Improves hippocampal damage in mice with insomnia and anxiety; (6) Increase the level of γ-aminobutyric acid (GABA) in the hippocampus of mice with insomnia and anxiety; (7) Increase the level of 5-hydroxytryptamine (5-HT) in the hippocampus of mice with insomnia and anxiety; (8) Reduce the level of dopamine (DA) in the hippocampus of mice with insomnia and anxiety; (9) Reduce the level of norepinephrine (NE) in the hippocampus of mice with insomnia and anxiety; (10) Reduce serum interleukin-1β (IL-1β) levels in mice with insomnia and anxiety; (11) Reduce the serum level of interleukin-6 (IL-6) in mice with insomnia and anxiety; (12) Reduce the serum level of tumor necrosis factor-α (TNF-α) in mice with insomnia and anxiety; (13) Increase the serum level of interleukin-10 (IL-10) in mice with insomnia and anxiety.

[0026] This invention has verified through clinical trials that a functional food composed of Ganoderma lucidum extract, Salvia miltiorrhiza extract, Astragalus membranaceus extract, jujube extract, Anemarrhena asphodeloides extract, and Cyperus rotundus extract has the effect of relieving insomnia accompanied by anxiety, specifically manifested in: (1) Reduce the Pittsburgh Sleep Quality Index (PSQI) score in people with insomnia and anxiety; (2) Reduce the Insomnia Severity Index (ISI) score in people with insomnia and anxiety; (3) Reduce the Epworth Sleepiness Scale (ESS) score in people with insomnia and anxiety; (4) Reduce the Generalized Anxiety Scale (GAD-7) score in people with insomnia and anxiety; (5) Reduce the self-rating depression scale (PHQ-9) score in people with insomnia and anxiety; Therefore, the functional food of this invention has broad application prospects in improving sleep disorders, relieving anxiety, regulating nerve homeostasis, and reducing oxidative inflammation in the body. Attached Figure Description

[0027] Figure 1 Flowchart for animal modeling intervention; Figure 2 The changes in body weight of mice in different groups of experiments; Figure 3 The sleep latency and sleep duration of mice in different groups were measured. Figure 4 Behavioral trajectory diagrams of mice from different groups in an open field experiment; Figure 5 The behavioral trajectory diagrams of different groups of experimental mice in the elevated cross maze; Figure 6 Anxiety index of mice in different groups; Figure 7 HE-stained sections of the hippocampus from different groups of experimental mice; Figure 8 The content of GABA in the hippocampus tissue of mice in different groups of experiments; Figure 9The content of 5-HT in the hippocampus tissue of mice in different groups of experiments; Figure 10 The content of DA in the hippocampus tissue of mice in different groups of experiments; Figure 11 The content of NE in the hippocampus tissue of mice in different groups of experiments; Figure 12 The serum IL-1β levels in mice from different experimental groups; Figure 13 The serum IL-6 levels in mice from different groups of experiments; Figure 14 Serum TNF-α levels in mice from different experimental groups; Figure 15 The serum IL-10 content of mice in different groups of experiments; Figure 16 PSQI scores at weeks 0 and 4 for patients in different groups; Figure 17 ISI scores at weeks 0, 2, and 4 for patients in different groups; Figure 18 ESS scores at weeks 0, 2, and 4 for patients in different groups; Figure 19 GAD-7 scores at weeks 0, 2, and 4 for patients in different groups; Figure 20 PHQ-9 scores at weeks 0, 2, and 4 for patients in different groups; Figure 21 This is a flowchart of a clinical trial process. Detailed Implementation

[0028] The present invention will now be described in detail with reference to the accompanying drawings and embodiments.

[0029] The p-chlorophenylalanine (PCPA) used in the following examples was purchased from Shanghai Haoyuan Biomedical Technology Co., Ltd.

[0030] The sodium pentobarbital used in the following examples was obtained from the Animal Experiment Center of Jiangnan University.

[0031] The functional food ingredients involved in the following examples—Ganoderma lucidum extract, Salvia miltiorrhiza extract, Astragalus membranaceus extract, Jujube extract, Anemarrhena asphodeloides extract, Cyperus rotundus extract, Ziziphus jujuba var. spinosa extract, and Gardenia jasminoides extract—were all purchased from Bofeimei Technology Co., Ltd.

[0032] The preparation method of the composition involved in the following examples is as follows: PCPA solution: Weigh 3.5g of PCPA powder and dissolve it in 100 mL of DMSO to prepare a PCPA solution with a concentration of 35 mg / mL.

[0033] Sodium pentobarbital solution: Weigh 55 mg of sodium pentobarbital powder and dissolve it in 10 mL of sterile physiological saline to prepare a sodium pentobarbital solution with a concentration of 55 mg / kg.

[0034] Functional Food 1: Prepare Functional Food Solution 1 by mixing 5.8 parts of Ganoderma lucidum extract, 5.3 parts of Salvia miltiorrhiza extract, 5.0 parts of Astragalus membranaceus extract, 3.3 parts of jujube extract, 3.3 parts of Anemarrhena asphodeloides extract, and 2.5 parts of Cyperus rotundus extract in sterile physiological saline.

[0035] Functional Food 2: Prepare functional food solution 2 by mixing 5.8 parts of Ganoderma lucidum extract, 5.3 parts of Salvia miltiorrhiza extract, 5.0 parts of Astragalus membranaceus extract, 3.3 parts of jujube extract, 3.3 parts of Ziziphus jujuba var. spinosa extract, and 2.5 parts of Gardenia jasminoides extract in sterile saline solution.

[0036] Example 1: Results of animal experiments simulating insomnia accompanied by anxiety The specific steps are as follows: Twenty-four SPF-grade male ICR mice (8 weeks old, 20-25 g) were randomly divided into four groups of six mice each: blank group, model group, functional group 1 (functional food 1), and functional group 2 (functional food 2). The mice were housed at the Experimental Animal Center of Jiangnan University at a constant temperature of 21°C. 26℃, humidity 40% 70%, noise level less than or equal to 60 dB, animal illumination 15 20LX (All animal experimental procedures were reviewed and approved by the Animal Welfare and Ethics Management Committee of Jiangnan University).

[0037] The experiment lasted a total of 28 days: the detailed experimental modeling and intervention flowchart is as follows. Figure 1 The animal experimental grouping, modeling, and intervention measures are shown in Table 1. Days 7-0 were the baseline / adaptation period for mice; days 0-21 were the modeling period for mice. From day 0-5, mice were injected intraperitoneally with 0.2 mL of 35 mg / kg PCPA solution daily. From day 0-21, mice were stimulated with a wooden clip for 5 min daily. From day 7-21, mice were administered gavage daily. Mice in the blank group and model group were administered 200 μL of sterile saline solution daily. Mice in functional group 1 were administered 200 μL of functional food 1 solution daily, and mice in functional group 2 were administered 200 μL of functional food 2 solution daily.

[0038] Table 1

[0039] Modeling Procedures: Insomnia Modeling: From day 0-5, mice in the model group, functional group 1, and functional group 2 were intraperitoneally injected with 35 mg / kg PCPA solution. 24 hours after PCPA injection, the insomnia model mice exhibited loss of circadian rhythm, continuous daytime activity, increased excitability and aggression, decreased appetite, and dull, disheveled fur, indicating successful modeling of the insomnia mouse model. Stress and Anxiety Modeling: From day 0-21, mice in the model group, functional group 1, and functional group 2 were housed together in a group. At a fixed time each day, the mice's tails were continuously stimulated with sterile wooden clips for 5 minutes. The blank control group received no tail-clamping stimulation and was housed normally. After 21 days of continuous intervention, stable anxiety and stress-related injury characteristics were observed, indicating successful modeling of the anxiety and stress.

[0040] Example 2: Effects of functional foods on body weight in mice with insomnia and anxiety During the animal experiments, the mouse weight was recorded weekly. The mouse weight (g) results are shown in Table 2 and... Figure 2 As shown: Table 2

[0041] The experimental results are shown in Table 2 and Figure 2 As shown, intraperitoneal injection of PCPA and chronic tail clamping stimulation caused weight loss in mice. Compared with the model group, both functional groups 1 and 2 effectively alleviated the weight loss in mice caused by insomnia accompanied by anxiety, and functional group 1 had a better alleviating effect than functional group 2, and its weight was closer to that of the control group mice.

[0042] Example 3: Effects of functional foods on sleep latency and sleep duration in mice with insomnia and anxiety The specific methods are as follows: The righting reflex test using sodium pentobarbital was used to evaluate the sedative-hypnotic effect of functional foods on mice with insomnia and anxiety. Mice were pretreated with the functional food by gavage for 30 min, followed by intraperitoneal injection of 55 mg / kg sodium pentobarbital. The time of sodium pentobarbital administration, the time of loss of the righting reflex, and the time of anesthesia recovery were recorded. The loss of the righting reflex was defined as the inability of the mouse to spontaneously return to an upright position within 60 seconds after being placed supine. The time interval from sodium pentobarbital injection to the loss of the righting reflex was used as the sleep latency, and the time interval from the loss of the righting reflex to spontaneous awakening was used as the sleep duration. This was used to assess the regulatory effect of functional foods on the sleep onset speed and sleep duration in mice with insomnia and anxiety. The results are as follows: Figure 3 As shown.

[0043] The results showed that the average sleep latency in the control group was 1.84±0.04 min, and the average sleep duration was 109.40±3.76 min. Mice in the control group fell asleep quickly, had a longer sleep duration, and exhibited good basal sleep. Compared with the control group, the sleep latency in the model group was significantly prolonged to 3.22±0.08 min, and the sleep duration was significantly shortened to 50.70±4.21 min. This suggests that the insomnia-anxiety model significantly prolongs sleep onset time and shortens sleep maintenance time, resulting in a typical insomnia phenotype characterized by difficulty falling asleep and impaired sleep maintenance. After functional food intervention, the sleep latency in functional group 1 mice decreased to 2.27±0.07 min, and the sleep duration recovered to 103.08±2.74 min; the sleep latency in functional group 2 mice was 2.56±0.08 min, and the sleep duration was 94.87±3.01 min. Both groups of functional foods can significantly shorten the sleep latency and prolong the sleep duration in model mice, and improve the insomnia symptoms in mice. Among them, the sedative-hypnotic effect of functional group 1 in shortening the sleep latency and prolonging the sleep duration is better than that of functional group 2.

[0044] The results of the righting reflex experiment with sodium pentobarbital above indicate that insomnia accompanied by anxiety significantly prolongs the sleep latency and shortens the sleep duration in mice. This functional food has clear sedative-hypnotic activity, which can accelerate the sleep onset speed and prolong the sleep duration in model mice, effectively improve the sleep disorder state of mice with insomnia and anxiety, and the intervention effect of functional group 1 is better.

[0045] Example 4: Effects of functional foods on the distance mice with insomnia and anxiety move in an open field test grid The specific method is as follows: The open field test (OFT) was used to evaluate the effect of functional food on anxiety-like behavior in mice with insomnia and anxiety. The open field device consisted of four independent chambers, each measuring 30 × 30 × 35 cm³. Mice were allowed to acclimatize to the environment for 5 minutes, followed by 5 minutes of behavioral video recording. The total movement distance and the distance traveled in the central area were recorded. The distance traveled in the central grid reflected the anxiety level of the mice, thus evaluating the effect of the functional food on improving the anxiety state of the mice. The results of the movement distance (cm) of the mice in the open field test are shown in Table 3, and the movement trajectory diagram is shown in... Figure 4 As shown.

[0046] The results showed that the total activity distance of the control group mice was 2687.91±315.41 cm, and the central grid distance reached 775.11±115.94 cm. The mice actively entered the open area in the center of the enclosure to explore, and their anxiety level was low. Compared with the control group, the total activity distance of the model group mice decreased to 2028.32±363.42 cm, and the central grid distance was only 337.46±31.35 cm. The activity range of the mice was significantly reduced, and they rarely entered the central area, preferring to move along the edge of the enclosure. This suggests that the insomnia-associated anxiety model mice exhibited significant anxiety-like behavior and obvious fear of open and unfamiliar environments. After functional food intervention, the total activity distance of the functional group 1 mice rebounded to 2431.99±512.67 cm, and the central grid distance increased to 545.23±55.21 cm; the total activity distance of the functional group 2 mice was 2398.33±454.77 cm, and the central grid distance was 544.08±54.25 cm. Both groups of mice showed a significantly increased central region activity distance compared to the model group, a marked recovery in their willingness to explore open areas, and relief of anxiety behavior. The improvement effect in functional group 1 was slightly better than that in functional group 2.

[0047] Motion trajectory diagram ( Figure 4 The data directly corroborates the above patterns: the tracks of mice in the blank group largely covered the central box area; the tracks of mice in the model group were concentrated around the edges of the box, with few tracks in the central area; after intervention in functional groups 1 and 2, the activity tracks of mice within the central grid increased significantly, and their exploration behavior in open areas was restored.

[0048] The above open field experiment results show that insomnia accompanied by anxiety inhibits mice's exploration behavior in the central open area and reduces the central activity distance; this functional food can significantly increase the movement distance of model mice in the central area of ​​the open field, improve the edge-seeking behavior of mice caused by anxiety, and has a good anti-anxiety effect, and the intervention effect of functional group 1 is better.

[0049] Table 3

[0050] Example 5: Effects of functional foods on the behavior of insomnia-associated anxiety mice in the open-arm region of an elevated cruciate maze. The specific method is as follows: The elevated cross maze test (EPM) was used to evaluate the effect of functional foods on anxiety-like behavior in mice with insomnia and anxiety. The maze consisted of two open arms, two closed arms (30 cm × 5 cm), and a central platform (5 cm × 5 cm). Mice were placed on the central platform of the maze to adapt for 1 minute, followed by 3 minutes of behavioral observation. The distance of the open arm movement, the duration of the open arm stay, and the number of times the arms were opened were recorded. The anxiety index of the mice was calculated based on these data. The behavioral data of the mice in the elevated cross maze test are shown in Table 4, and the movement trajectory diagram is shown in the figure below. Figure 5As shown, the anxiety index is as follows Figure 6 As shown.

[0051] The results showed that the control group mice entered the open arm 18.8±5.02 times, stayed in the open arm for 78.14±19.45s, and the total distance moved in the open arm was 386.86±177.25cm. The anxiety index was 43.69±1.96%, indicating that the mice preferred to enter the open arm area and had a lower anxiety level. Compared with the control group, the model group mice entered the open arm only 7.8±1.80 times, stayed in the open arm for 12.44±3.73s, and the distance moved in the open arm was 36.73±12.56cm. The anxiety index increased significantly to 81.72±2.56%, indicating that the mice rarely entered the open arm and preferred the closed arm, suggesting that the insomnia-associated anxiety model mice exhibited significant anxiety-like behavior. Compared to the model group, mice in functional group 1 showed a significant increase in the number of times they opened their arms to enter the area, the duration of their stay, and the distance they moved with their arms open, while their anxiety index decreased to 66.22±2.32%. In functional group 2, all indicators of their arm-opening behavior improved simultaneously, with an anxiety index of 66.97±2.10%. Both groups of functional foods significantly enhanced mice's exploration behavior in the arm-opening area, reduced their anxiety index, and alleviated their anxiety. The anti-anxiety effect of functional group 1 was slightly better than that of functional group 2.

[0052] Motion trajectory diagram ( Figure 5 The above pattern is visually confirmed: the tracks of mice in the blank group were mostly distributed in the open arm; the tracks of mice in the model group were almost only concentrated in the closed arm and the central platform; after functional food intervention, the activity tracks of mice in functional group 1 and functional group 2 increased significantly in the open arm, and their willingness to explore open areas was restored.

[0053] The results of the elevated cross maze experiment above show that insomnia accompanied by anxiety significantly inhibits mice’s exploration behavior in open environments and greatly increases the anxiety index. This functional food can effectively improve mice’s open-arm exploration behavior, reduce the anxiety index, and improve the anxiety-like behavior of model mice. It has clear anti-anxiety activity, and the intervention effect of functional group 1 is better.

[0054] Table 4

[0055] Example 6: Effects of functional foods on hippocampal pathological damage in mice with insomnia and anxiety The specific method is as follows: Mice were anesthetized with isoflurane 1 hour after the last administration following 28 days of continuous intervention. Blood was collected from the orbital venous plexus, and the mice were immediately euthanized after blood collection. Whole brain tissue was rapidly dissected on an ice plate, fixed in 4% paraformaldehyde solution, and embedded in paraffin to prepare continuous tissue sections with a thickness of 4 μm. The sections were dewaxed with xylene, dehydrated with graded ethanol to distilled water, and then stained with hematoxylin and eosin (HE). The improvement of hippocampal tissue pathological damage in mice with insomnia and anxiety was observed through brain tissue pathological staining. The results are as follows: Figure 7 As shown.

[0056] The results showed that in the control group, the neurons in the CA1 region of the hippocampus were densely arranged, clearly layered, with intact cell morphology, plump and uniformly stained nuclei, and no obvious cell shrinkage, vacuolar degeneration, or inflammatory infiltration. The hippocampal tissue morphology and structure were intact. Compared with the control group, the model group mice showed obvious pathological damage in the CA1 region of the hippocampus: neurons were loosely and disordered, a large number of cells showed shrunken and deeply stained structures, cell bodies were shrunken, intercellular spaces were enlarged, and obvious vacuolar degeneration was visible, suggesting that the insomnia-anxiety model can induce hippocampal neuronal damage and neuronal apoptosis in mice. After intervention with functional foods, the pathological damage in the hippocampus of mice in both functional groups 1 and 2 was significantly alleviated: the regularity of neuronal arrangement was significantly restored, the number of shrunken and degenerated cells was greatly reduced, and the cell morphology tended to be intact; among them, the hippocampal neurons of mice in functional group 1 were more intact, and the neural tissue repair effect was better than that in functional group 2.

[0057] The above HE staining pathological results indicate that insomnia accompanied by anxiety causes degenerative damage to hippocampal neurons in mice, disrupting the normal tissue structure of the hippocampus. This functional food can effectively reduce pathological changes such as degeneration and shrinkage of hippocampal neurons in model mice, protect the integrity of hippocampal neurons, and alleviate central brain tissue damage induced by anxiety and insomnia. Moreover, the neuroprotective effect of functional group 1 is better.

[0058] Example 7: Effects of functional foods on GABA content in the hippocampus of mice with insomnia and anxiety The specific method is as follows: After the experiment, mouse brain tissue was rapidly dissected on ice, and mouse hippocampal tissue was accurately isolated and obtained into 1.5 mL of enzyme-free EP. Pre-chilled PBS (weight-to-volume ratio of 1:9) was added, and the mixture was thoroughly homogenized. The homogenate was centrifuged at 4℃ and 12000 r / min for 10 min to obtain the tissue supernatant. The supernatant was aspirated into enzyme-free PCR tubes, aliquoted, and stored at -80℃. The GABA content in mouse hippocampal tissue was detected according to the instructions of the mouse γ-aminobutyric acid (GABA) ELISA quantitative detection kit. The results are as follows. Figure 8 As shown.

[0059] The results showed that the hippocampal GABA level in the control group was 62.76±4.80 ng / L, in the model group it was 26.14±3.97 ng / L, in functional group 1 it was 51.74±2.67 ng / L, and in functional group 2 it was 49.37±2.66 ng / L. Compared with the control group, the hippocampal GABA content in the model group was significantly decreased, with a decrease of 58.35%, suggesting that the insomnia-anxiety model causes a large depletion of the inhibitory neurotransmitter GABA in the hippocampus of mice, resulting in impaired central inhibitory function. Compared with the model group, the hippocampal GABA content in functional group 1 was significantly increased, with an increase of 97.93%; the hippocampal GABA content in functional group 2 was also significantly increased compared with the model group, with an increase of 88.87%. Both functional food groups significantly increased the GABA content in hippocampal tissue and alleviated GABA neurotransmitter loss in model mice, with functional group 1 showing a better effect than functional group 2.

[0060] The above experimental results indicate that GABA is a key inhibitory neurotransmitter in the central nervous system, and insufficient GABA content in the hippocampus is an important mechanism for inducing insomnia and anxiety in mice. The insomnia-anxiety model significantly reduces GABA levels in the hippocampus, disrupting the central excitation-inhibition balance. This functional food can effectively upregulate GABA concentration in the hippocampus of mice with insomnia and anxiety, and restore inhibitory neurotransmitter homeostasis, with the improvement effect being better in functional group 1.

[0061] Example 8: Effects of functional foods on 5-HT content in hippocampal tissue of mice with insomnia and anxiety The specific method is the same as in Example 7. The 5-HT content in mouse hippocampal tissue was detected according to the instructions of the mouse 5-HT ELISA quantitative detection kit. The results are as follows: Figure 9 As shown.

[0062] The results showed that the hippocampal 5-HT level in the control group was 45.73±3.85 μg / L, in the model group it was 23.33±1.21 μg / L, in functional group 1 it was 38.75±1.12 μg / L, and in functional group 2 it was 37.64±1.74 μg / L. Compared with the control group, the hippocampal 5-HT content in the model group was significantly decreased, with a decrease of 48.98%, suggesting that the insomnia-anxiety model causes a large consumption of hippocampal 5-HT neurotransmitters and impairs central mood regulation function in mice. Compared with the model group, the hippocampal 5-HT content in functional group 1 was significantly increased, with an increase of 66.10%; the hippocampal 5-HT content in functional group 2 was also significantly increased compared with the model group, with an increase of 61.34%. Both functional food groups significantly increased the 5-HT content in hippocampal tissue and alleviated the loss of 5-HT neurotransmitters in model mice, with functional group 1 showing a better effect than functional group 2.

[0063] The above experimental results indicate that 5-HT is a key neurotransmitter in the central regulation of sleep and anxiety, and that hippocampal 5-HT deficiency is an important mechanism for inducing insomnia and anxiety-like behavior in mice. The insomnia-anxiety model significantly reduces hippocampal 5-HT levels, disrupting central mood and sleep homeostasis. This functional food can effectively upregulate 5-HT concentration in the hippocampus of mice with insomnia and anxiety, restoring the balance of 5-HT neurotransmitters, with functional group 1 showing even better improvement.

[0064] Example 9: Effects of functional foods on DA content in the hippocampus of mice with insomnia and anxiety The specific method is the same as in Example 7. The DA content in mouse hippocampal tissue was detected according to the instructions of the mouse dopamine (DA) ELISA quantitative detection kit. The results are as follows: Figure 10 As shown.

[0065] The results showed that the hippocampal dopamine (DA) level in the control group was 7.42±0.73 μg / L, in the model group it was 13.63±1.18 μg / L, in functional group 1 it was 8.59±0.33 μg / L, and in functional group 2 it was 8.96±0.61 μg / L. Compared with the control group, the model group showed a significant increase in hippocampal DA content, with an increase of 83.69%, suggesting that the insomnia-anxiety model causes excessive accumulation of dopamine neurotransmitters in the hippocampus of mice, leading to dysfunction of central excitation regulation. Compared with the model group, functional group 1 showed a significant decrease in hippocampal DA content, with a reduction of 36.98%. Functional group 2 also showed a significant decrease in hippocampal DA content, with a reduction of 34.26%. Both functional food groups significantly reduced the abnormally elevated DA content in the hippocampus and improved the dopamine neurotransmitter disorder in the model mice, with functional group 1 showing a better downregulation effect than functional group 2.

[0066] The above experimental results indicate that dopamine (DA) is a key neurotransmitter mediating central excitation, stress, and anxiety. Excessive accumulation of DA in the hippocampus is an important mechanism for inducing insomnia and anxiety-induced hyperactivity in mice. The insomnia-anxiety model significantly increases DA levels in the hippocampus, disrupting the central excitatory-inhibitory neurotransmitter balance. This functional food can effectively downregulate the abnormally elevated DA concentration in the hippocampus of insomnia-anxiety mice, restore dopamine neurotransmitter homeostasis, and the improvement effect is even better in functional group 1.

[0067] Example 10: Effects of functional foods on NE content in the hippocampus of mice with insomnia and anxiety The specific method is the same as in Example 7. The NE content in mouse hippocampal tissue was detected according to the instructions of the mouse norepinephrine (NE) ELISA quantitative detection kit. The results are as follows: Figure 11 As shown.

[0068] The results showed that the norepinephrine (NE) level in the hippocampus of mice in the control group was 4.04±0.41 μg / L, in the model group it was 6.91±0.47 μg / L, in functional group 1 it was 5.28±0.32 μg / L, and in functional group 2 it was 5.17±0.50 μg / L. Compared with the control group, the NE content in the hippocampus of the model group was significantly increased, with an increase of 71.04%, suggesting that the insomnia-anxiety model causes excessive release of norepinephrine neurotransmitters in the hippocampus of mice, resulting in an imbalance between central stress and excitation regulation. Compared with the model group, the NE content in the hippocampus of functional group 1 was significantly decreased, with a reduction of 23.59%; the NE content in the hippocampus of functional group 2 was also significantly reduced compared with the model group, with a reduction of 25.18%. Both functional food groups were able to significantly reduce the abnormally elevated NE content in the hippocampus and alleviate the norepinephrine neurotransmitter disorder in the model mice. The downregulation effect of functional group 2 was slightly better than that of functional group 1.

[0069] The above experimental results indicate that norepinephrine (NE) is a key neurotransmitter mediating central stress, anxiety, and arousal. Excessive NE elevation in the hippocampus is a significant contributing factor to persistent insomnia and agitation in mice. The insomnia-anxiety model significantly increases NE levels in the hippocampus, disrupting the balance between excitatory and inhibitory neurotransmitters in the central nervous system. Functional group 1 effectively downregulated the abnormally elevated NE concentration in the hippocampus of insomnia-anxiety mice, restored norepinephrine neurotransmitter homeostasis, and alleviated the stress-induced agitation in the model mice.

[0070] Example 11: Effects of dietary supplements on serum IL-1β levels in mice with insomnia and anxiety The specific method is as follows: After the experiment, blood was collected from the orbital cavity of mice and placed in 1.5 mL enzyme-free EP tubes. The blood was allowed to stand for at least 2 hours, and then centrifuged at 4℃ and 3000 r / min for 15 min to obtain serum. The serum was carefully aspirated into enzyme-free PCR tubes, aliquoted, and stored at -80℃. The IL-1β content in mouse serum was detected according to the instructions of the mouse interleukin 1β (IL-1β) ELISA quantitative detection kit. The results are as follows. Figure 12 As shown.

[0071] The results showed that the serum IL-1β level in the control group was 162.42±5.86 pg / mL, the serum IL-1β level in the model group was 288.43±10.53 pg / mL, the serum IL-1β level in functional group 1 was 198.07±9.77 pg / mL, and the serum IL-1β level in functional group 2 was 205.93±9.48 pg / mL. Compared with the control group, the serum pro-inflammatory factor IL-1β level in the model group was significantly increased, with an increase of 77.58%, suggesting that the insomnia-anxiety model can induce a systemic inflammatory response in mice, resulting in a large release of peripheral inflammatory factors. Compared with the model group, the serum IL-1β level in functional group 1 was significantly decreased, with a reduction of 31.33%. Compared with the model group, the serum IL-1β level in functional group 2 was also significantly downregulated, with a reduction of 28.60%. Both functional food groups were able to significantly reduce the abnormally elevated IL-1β levels in the peripheral regions of model mice and alleviate inflammatory damage in the body. Among them, the anti-inflammatory effect of functional group 1 was better than that of functional group 2.

[0072] The above experimental results indicate that IL-1β is a key pro-inflammatory cytokine. Elevated peripheral inflammation levels further aggravate central nervous system disorders and exacerbate insomnia and anxiety-like behaviors in mice. The insomnia-anxiety model significantly increases serum IL-1β concentration, inducing systemic low-grade inflammation. This functional food can effectively downregulate excessively high serum IL-1β in mice with insomnia and anxiety, inhibit excessive inflammatory responses, and reduce inflammation-mediated sleep and mood impairment. The intervention effect of functional group 1 is even better.

[0073] Example 12: Effects of functional foods on serum IL-6 levels in mice with insomnia and anxiety The specific method is the same as in Example 11. The IL-6 content in mouse serum was detected according to the instructions of the mouse interleukin-6 (IL-6) ELISA quantitative detection kit. The results are as follows: Figure 13 As shown.

[0074] The results showed that the serum IL-6 level in the control group was 75.24±12.17 pg / mL, the serum IL-6 level in the model group was 361.30±14.59 pg / mL, the serum IL-6 level in functional group 1 was 137.09±10.06 pg / mL, and the serum IL-6 level in functional group 2 was 137.64±16.36 pg / mL. Compared with the control group, the serum pro-inflammatory factor IL-6 level in the model group was significantly increased, with an increase of 380.20%, suggesting that the insomnia-anxiety model can induce a severe peripheral inflammatory response in mice, releasing a large amount of the inflammatory mediator IL-6. Compared with the model group, the serum IL-6 level in functional group 1 was significantly decreased, with a reduction of 62.05%; the serum IL-6 level in functional group 2 was also significantly downregulated compared with the model group, with a reduction of 61.90%. Both functional food groups were able to significantly reduce the abnormally elevated IL-6 levels in the peripheral regions of model mice and effectively alleviate excessive inflammatory damage in the body. The intervention effects of the two groups were similar, with functional group 1 being slightly better than functional group 2.

[0075] The above experimental results indicate that IL-6 is a core pro-inflammatory factor mediating systemic low-grade inflammation and neuroinflammation. Abnormally elevated peripheral IL-6 can cross the blood-brain barrier, disrupting the balance of central neurotransmitters and exacerbating insomnia and anxiety in mice. In the insomnia-anxiety model, serum IL-6 concentration is significantly increased, inducing persistent inflammatory stress. This functional food can significantly downregulate excessively high IL-6 levels in the serum of mice with insomnia and anxiety, effectively inhibiting the body's inflammatory stress response and blocking inflammation-mediated sleep and mood disorder pathways.

[0076] Example 13: Effects of functional foods on serum TNF-α levels in mice with insomnia and anxiety The specific method is the same as in Example 11. The TNF-α content in mouse serum was detected according to the instructions of the mouse tumor necrosis factor α (TNF-α) ELISA quantitative detection kit. The results are as follows: Figure 14 As shown.

[0077] The results showed that the serum TNF-α level in the control group was 115.15±8.18 pg / mL, the serum TNF-α level in the model group was 213.78±12.22 pg / mL, the serum TNF-α level in functional group 1 was 142.87±5.40 pg / mL, and the serum TNF-α level in functional group 2 was 157.28±9.92 pg / mL. Compared with the control group, the serum pro-inflammatory factor TNF-α level in the model group was significantly increased, with an increase of 85.65%, suggesting that the insomnia-anxiety model activates systemic inflammatory pathways in mice, releasing large amounts of tumor necrosis factor TNF-α and inducing inflammatory stress. Compared with the model group, the serum TNF-α level in functional group 1 was significantly decreased, with a reduction of 33.17%; the serum TNF-α level in functional group 2 was also significantly downregulated compared with the model group, with a reduction of 26.43%. Both functional food groups were able to significantly reduce the abnormally elevated TNF-α levels in the peripheral regions of model mice and alleviate the systemic inflammatory response. Among them, functional group 1 showed better anti-inflammatory effects than functional group 2.

[0078] The above experimental results indicate that TNF-α is a core pro-inflammatory factor that initiates the body's inflammatory cascade response. Excessive release of peripheral TNF-α induces neuroinflammation, disrupts the balance of central neurotransmitters, and exacerbates insomnia and anxiety-like behaviors in mice. The insomnia-anxiety model significantly increases serum TNF-α concentration, causing persistent inflammatory damage. This functional food can effectively downregulate excessively high levels of TNF-α in the serum of mice with insomnia and anxiety, inhibit the amplification effect of the inflammatory cascade, and alleviate inflammation-mediated sleep disorders and mood disturbances, with the intervention effect of functional group 1 being even better.

[0079] Example 14: Effects of functional foods on serum IL-10 levels in mice with insomnia and anxiety The specific method is the same as in Example 11. The IL-10 content in mouse serum was detected according to the instructions of the mouse interleukin-10 (IL-10) ELISA quantitative detection kit. The results are as follows: Figure 15 As shown.

[0080] The results showed that the serum IL-10 level in the blank control group was 113.47±3.84 pg / mL, the serum IL-10 level in the model group was 67.94±2.60 pg / mL, the serum IL-10 level in functional group 1 was 91.61±5.30 pg / mL, and the serum IL-10 level in functional group 2 was 84.72±2.37 pg / mL. Compared with the blank control group, the serum anti-inflammatory factor IL-10 level in the model group was significantly decreased, with a decrease of 40.12%, suggesting that the insomnia-anxiety model inhibits the secretion of anti-inflammatory factors in mice, impairs the body's anti-inflammatory compensatory ability, and fails to effectively antagonize the excessive inflammatory response. Compared with the model group, the serum IL-10 level in functional group 1 was significantly increased, with an increase of 34.84%; the serum IL-10 level in functional group 2 was also significantly increased compared with the model group, with an increase of 24.70%. Both functional food groups were able to significantly increase the level of the anti-inflammatory factor IL-10 in the serum of model mice and restore the body's anti-inflammatory balance. Among them, functional group 1 was more effective than functional group 2 in increasing IL-10 secretion.

[0081] The above experimental results indicate that IL-10 is a core anti-inflammatory cytokine in the body, which can inhibit the release of pro-inflammatory factors such as IL-1β, IL-6, and TNF-α, and alleviate systemic and central nervous system inflammation. The insomnia-anxiety model significantly reduced serum IL-10 concentration, impairing the anti-inflammatory protective mechanism, and the continued inflammation exacerbated sleep and mood disorders. This functional food can effectively upregulate serum IL-10 levels in mice with insomnia and anxiety, enhance the body's endogenous anti-inflammatory capacity, and improve insomnia and anxiety-related symptoms in mice through anti-inflammatory pathways, with functional group 1 showing even better intervention effects.

[0082] Example 15: Randomized, double-blind, placebo-controlled clinical trial I. The specific sample standards in this embodiment are as follows: 1. Selection Criteria The diagnostic criteria for chronic insomnia in Western medicine are jointly formulated with reference to the diagnostic criteria for chronic insomnia in the International Classification of Sleep Disorders, Third Edition (ICSD-3) and the Chinese Guidelines for the Diagnosis and Treatment of Insomnia (2025 Edition).

[0083] ① Subjective complaints of a significant decline in the quality or quantity of sleep, accompanied by at least one of the following symptoms: a. difficulty falling asleep; b. difficulty maintaining sleep, manifested as frequent awakenings or difficulty falling back asleep after waking up; c. early awakening and inability to fall back asleep; d. coexisting medical conditions; ② Sleep disturbances (or related daytime dysfunction) significantly interfere with daily activities, affecting social, daily life, work, study and other social functions; ③ The above-mentioned insomnia problems occur at least three times a week and persist for more than three months; ④ The above symptoms cannot be explained by other sleep disorders (such as hypersomnia, breathing-related sleep disorders, sleep-wake rhythm disorders, and parasomnias) and do not occur during the course of other sleep disorders; ⑤ Sleep is not caused by the physiological effects of substances (such as substance abuse).

[0084] Individuals must meet all of the following criteria to be eligible to participate in the trial: (1) Meets the Western medical diagnostic criteria for chronic insomnia; (2) Age range is between 18 and 65 years old, gender is not limited; (3) PSQI score is >7 before enrollment, GAD-7 score is <15, and PHQ-9 score is <15; (4) Subjects can understand the content of the scale and follow the treatment, and have no communication or cognitive impairment; (5) Subjects are aware of the research project and process and voluntarily sign the informed consent form.

[0085] 2. Exclusion criteria Individuals meeting any of the following criteria will be excluded from this trial: (1) Having other types of severe sleep disorders, such as severe sleep apnea syndrome (STOP-Bang score ≥4 points), severe periodic limb movement disorder, etc.; (2) Meeting the diagnostic criteria for major mental illnesses in the DSM-5 criteria as assessed by a psychiatrist, including anxiety disorders, depressive disorders, bipolar disorder, schizophrenia and other severe mental disorders; (3) Having serious primary diseases of the heart, brain, liver, kidneys and hematopoietic system, (4) Those who have taken any antidepressants, antipsychotics, sedatives or hypnotics within one week before formal enrollment, or who have consumed excessive alcohol within one week before formal enrollment; (5) Those who have worked shifts, traveled long distances across time zones, or had significant sleep disturbances within two weeks before formal enrollment; those who have experienced major life stress events (divorce, bereavement, major surgery, etc.) within the past month; (6) Women who are pregnant or breastfeeding; (7) Those who are allergic or intolerant to functional foods (Ganoderma lucidum, Astragalus membranaceus, Salvia miltiorrhiza, jujube, Anemarrhena asphodeloides, Cyperus rotundus); (8) Those who have cognitive impairment and cannot cooperate in completing the scale assessment, or those who cannot guarantee that they will not use other sleep aids without authorization during the trial period.

[0086] 3. Criteria for quitting midway (1) Cases that do not meet the inclusion criteria but are mistakenly included; (2) Subjects with poor compliance who do not take functional foods as prescribed during treatment or add drugs or other treatments that may affect the efficacy without authorization.

[0087] 4. Shedding Standard (1) The patient needs to withdraw from the trial after a professional evaluation by the doctor; (2) The patient voluntarily requests to withdraw from the trial.

[0088] II. Patient Grouping and Intervention All patients recruited in this embodiment have signed informed consent forms and have received approval from the Ethics Committee of Wuxi Mental Health Center. The recruitment process and grouping in this embodiment are as follows: Figure 21 As shown, a total of 116 patients with chronic insomnia and anxiety were recruited and randomly divided into two groups using a simple randomization method: (1) Plant extract powder group: Take plant extract powder for 4 weeks (drink 1 sachet warm every night); (2) Placebo group: Take placebo for 4 weeks (one sachet each night).

[0089] The product consists of two parts: a plant extract powder (3 g / sachet) containing the following ingredients (by weight): 0.58 g Ganoderma lucidum extract, 0.53 g Salvia miltiorrhiza extract, 0.50 g Astragalus membranaceus extract, 0.33 g Ziziphus jujuba extract, 0.33 g Anemarrhena asphodeloides extract, 0.25 g Cyperus rotundus extract, 0.02 g Steviosides, and 0.48 g Maltodextrin; and a placebo (3 g / sachet) containing the following ingredients (by mass fraction): 0.02 g Steviosides and 2.98 g Maltodextrin. The probiotic powder and placebo are identical in packaging and appearance and are both manufactured by Glerui (Wuxi) Nutrition Technology Co., Ltd.

[0090] III. Research Steps and Related Inspections (1) Patients were scored on the scale at weeks 0, 2 and 4, and the changes in each indicator were recorded; (2) Blood and stool samples were collected from patients before intervention (baseline) and at the end of week 4. (3) Patients need to be followed up in the 2nd and 4th weeks and report symptoms and adverse events to the doctor.

[0091] IV. Endpoint Indicators 1. Primary endpoint: The effect of plant extract powder versus placebo on improving chronic insomnia was evaluated by comparing the changes in PSQI scores from baseline at the end of week 4 in different groups of patients.

[0092] 2. Secondary endpoint: (1) The effect of plant extract powder on improving the severity of insomnia compared with placebo was evaluated by comparing the changes in ISI scores at the end of the second and fourth weeks of different groups of patients from the baseline score.

[0093] (2) The effect of plant extract powder on improving daytime sleepiness and daytime mental state compared with placebo was evaluated by comparing the changes in ESS scores at the end of the second and fourth weeks of different groups of patients from the baseline score.

[0094] (3) The effect of plant extract powder on improving generalized anxiety disorder was evaluated by comparing the changes in GAD-7 scores at the end of the second and fourth weeks of different groups of patients compared with baseline scores.

[0095] (4) The effect of plant extract powder on improving depressive mood compared with placebo was evaluated by comparing the changes in PHQ-9 scores at the end of the second and fourth weeks of different groups of patients from the baseline score.

[0096] (5) Safety analysis of plant extract powder.

[0097] V. Statistical Analysis The effectiveness evaluation analysis used the Full Analysis Set (FAS), which included eligible cases and dropout cases. Safety indicators were analyzed using the Security Data Set (SS).

[0098] SPSS 27 and GraphPad Prism 10.1.2 statistical software were used to analyze baseline data and symptom improvement data. The Shapiro-Wilk test confirmed a normal distribution; the homogeneity of variance test also confirmed homogeneity; an independent samples t-test was used, and (Mean ± SD) was used for description. However, the data did not conform to a normal distribution, and the Mann-Whiteny U rank-sum test was used, with M( P25, P75 Unordered categorical data were analyzed using the χ² test and frequency description; descriptive measurement data were analyzed using two-way repeated measures ANOVA. Within-group differences at different visit time points within the same intervention group were analyzed using the Šidák multiple test, and between-group differences at the same visit time point between different intervention groups were analyzed using the Šidák or Tukey multiple comparison test. P <0.05 indicates a statistically significant difference, and ns indicates no difference within or between groups. Indicates within-group differences P <0.05, # indicates within-group difference P <0.05.

[0099] VI. Experimental Results 1. Patient Basic Information The final data included 58 participants in the plant extract powder group and 58 participants in the placebo group. Basic information of the included patients is shown in Table 5. There were no statistically significant differences in age, sex, BMI, and blood pressure between the two groups (p > 0.05), indicating that there were no significant differences in general characteristics between the two groups, and their baselines were comparable.

[0100] Table 5

[0101] a: The normality test (Shapiro Wilk test) shows that it conforms to a normal distribution; the homogeneity of variance test results show that the variances are homogeneous; an independent samples t-test is used, and the results are described using (Mean ± SD).

[0102] b: The result shows that the distribution does not conform to a normal distribution after a normality test. The Mann-Whiteny U rank-sum test is used, and M( P25， P75 )describe.

[0103] c: For unordered categorical data, the χ² test was used, and frequency was used for description.

[0104] Before treatment, there were no statistically significant differences in efficacy indicators (PSQI, ISI, ESS, PHQ-9) between the two groups (p > 0.05). Although there was a statistically significant difference in the total GAD-7 score (p < 0.001), the total GAD-7 score in the plant extract powder group was higher than that in the placebo group, and the baseline balance was comparable. A detailed comparison of the baseline balance of efficacy indicators between the two groups is shown in Table 6.

[0105] Table 6

[0106] a: The normality test (Shapiro Wilk test) shows that it conforms to a normal distribution; the homogeneity of variance test results show that the variances are homogeneous; an independent samples t-test is used, and the results are described using (Mean ± SD).

[0107] b: Since the normality test shows it does not conform to a normal distribution, the Mann-Whiteny U rank-sum test is used, and M( P25, P75 )describe.

[0108] 2. Effects of 4-week intervention with plant extract powder on patients' PSQI scores Repeated measures ANOVA with Greenhouse-Geisser correction was used to analyze the PSQI scores of 113 subjects (n=56 in the placebo group and n=57 in the plant extract powder group) at two visit sites in weeks 0 and 4. The results showed a main effect of group ( a P <0.0001), time main effect ( b P =0.0007) and the interaction effect between group and time ( c P The difference was statistically significant (<0.0001), indicating a difference in overall improvement of PSQI scores between the two interventions, with both groups showing a significant decrease in scores as the intervention duration increased. An interaction between group and time was observed, suggesting that the improvement magnitude of the two interventions varied significantly with the duration of treatment. Within-group Šidák multiple comparisons showed that PSQI scores in both groups were significantly lower than baseline after 4 weeks of intervention (<0.0001). (p < 0.0001) indicates that both interventions can reduce PSQI scores, and the interaction effect further demonstrates that the sleep improvement effect of plant extract powder is significantly better than that of placebo over time.

[0109] A comparison of the two intervention methods at different visit points was conducted between groups. The comparison results of the PSQI total scores of the two groups at different time points are shown in Table 7 below. It can be seen that at baseline in week 0, the PSQI scores of the two groups were 9 (10.5, 13) and 9 (12, 14), respectively, with no statistically significant difference between groups (p=0.392). Figure 16 It can be seen that the baseline distributions of the two groups were basically the same, and the insomnia levels of the subjects were comparable; after 4 weeks of intervention, the PSQI score of the placebo group was 7.27±3.49, and that of the plant extract powder group was 4 (2, 5), with highly significant differences between the groups. #### (p < 0.0001) Compared with the placebo group, the PSQI score of the plant extract powder group decreased by 44.98%, showing a greater improvement. An independent samples t-test was performed on the difference in PSQI scores (0-4 weeks) between the two interventions at two visit points. The mean difference in the placebo group was -3.93 ± 3.42, and the mean difference in the plant extract powder group was -8.16 ± 3.86, with statistically significant differences between the groups (p < 0.001). The decrease in PSQI score in the plant extract powder group was 107.63% greater than that in the placebo group. The inter-group comparison results of the week 4 visit point and the difference indicate that the plant extract powder of this invention is significantly more effective than the placebo in reducing PSQI scores and improving sleep quality. Summary Table 7 and Figure 16 The results showed that although both the placebo and the plant extract powder of the present invention could reduce the PSQI score and alleviate insomnia in the subjects after 4 weeks of intervention, the plant extract powder had a significantly greater effect on improving sleep quality than the placebo and had a stronger effect on improving insomnia.

[0110] Table 7

[0111] I. The normality test shows that it does not conform to a normal distribution. The Mann-Whiteny U rank-sum test is used, and the result is described using M(P25, P75).

[0112] II. The normality test (Shapiro Wilk test) shows that it conforms to a normal distribution, described using (Mean ± SD).

[0113] III. The differences between the different intervention groups at weeks 0 and 4 were analyzed using the Šidák test, and the marginal mean of LS was analyzed using the t-test.

[0114] IV. The differences between the different intervention groups (0-4 weeks) showed p>0.05 in the Shapiro-Wilk test, indicating a normal distribution. An independent samples t-test was then used.

[0115] V. a P This is due to the group effect. b P For time effect ， c P This is the interaction effect between group and time.

[0116] VI. For different visit sites within the same intervention group, use the Šidák multiple comparison test: compared to week 0, p < 0.0001.

[0117] 3. Effects of plant extract powder intervention on patients' ISI scores after 2-4 weeks. Repeated measures ANOVA with Greenhouse-Geisser correction was used to analyze the ISI scores of 113 subjects (n=56 in the placebo group and n=57 in the plant extract powder group) at three visit sites in weeks 0, 2, and 4. The results showed a main effect of group ( a P <0.0001), time main effect ( b P <0.0001) and the interaction effect between group and time ( c P The scores <0.0001 were statistically significant, indicating a difference in overall improvement in insomnia severity scores between the two interventions, with both groups showing a significant decrease in scores over time. An interaction between group and time was observed, suggesting that the degree of insomnia relief achieved by the two interventions varied significantly with the duration of treatment. Tukey multiple comparisons within the groups showed that the placebo group had a significantly lower ISI score at week 2 compared to baseline. p < 0.0001, and the level of decline remained significant in week 4 ( p < 0.01; the ISI scores of the plant extract powder group were significantly lower than baseline at weeks 2 and 4 after intervention (p < 0.01). p < 0.0001 indicates that both interventions can reduce the severity score of insomnia. The interaction effect further shows that the effect of plant extract powder in relieving the severity of insomnia is significantly better than that of placebo over the duration of intervention.

[0118] A comparison of the two intervention methods at different visit points was conducted between groups. Table 8 shows the comparison of the total ISI scores of the two groups at different time points. It can be seen that at baseline in week 0, the ISI scores of the two groups were 15.48±4.38 and 16.96±3.89, respectively, with no statistically significant difference between groups (p=0.299). Figure 17 It can be seen that the baseline score distributions of the two groups were basically consistent, and the baseline insomnia severity of the subjects was comparable. At week 2 of the intervention, the ISI score in the placebo group was 9 (8, 14.25), and in the plant extract powder group it was 10.11±4.60, with no statistically significant difference between the groups (p=0.556). After week 4 of the intervention, the ISI score in the placebo group was 12.50±6.48, and in the plant extract powder group it was 5 (1.75, 8), with a highly significant difference between the groups. #### (p < 0.0001) Compared with the placebo group, the plant extract powder group showed a 60% decrease in ISI score and a more significant reduction in insomnia severity. Independent samples t-tests were performed on the differences in ISI scores between the two interventions at 0-2 weeks and 0-4 weeks. The difference at 0-2 weeks was: the mean difference between the placebo group and the plant extract powder group was [value missing]. The average difference between the plant extract powder groups was 4.23 ± 6.38. The mean difference between groups was 6.86 ± 4.67 (p = 0.013); the difference between weeks 0 and 4: the mean difference in the placebo group was... The average difference between the plant extract powder groups was 2.98 ± 7.11. The difference between the groups was 11.7 ± 5.55, which was statistically significant (p < 0.01). The difference in ISI scores between the plant extract powder group and the placebo group decreased by 292.62% from week 0 to week 4. The comparison between the week 4 visit and the score difference from week 0 to week 4 together indicate that the plant extract powder of this invention is significantly more effective than the placebo in reducing the severity of insomnia scores and alleviating the severity of insomnia symptoms.

[0119] Combined with Table 8 Figure 17 The results showed that although both the placebo and the plant extract powder of the present invention could reduce the subject's ISI score and alleviate the severity of insomnia after 4 weeks of intervention, the plant extract powder's advantage in improving insomnia continued to increase with the extension of intervention time, and its overall efficacy in relieving insomnia symptoms was significantly stronger than that of the placebo.

[0120] Table 8

[0121] I. The normality test shows that it does not conform to a normal distribution. The Mann-Whiteny U rank-sum test is used, and the result is described using M(P25, P75).

[0122] II. The normality test (Shapiro Wilk test) shows that it conforms to a normal distribution, described using (Mean ± SD).

[0123] III. The differences between the different intervention groups at weeks 0, 2, and 4 were analyzed using the Šidák test, and the marginal mean of LS was analyzed using the t-test.

[0124] IV. The differences between the different intervention groups (0-2 weeks, 0-4 weeks) showed p > 0.05 in the Shapiro-Wilk test, indicating a normal distribution. An independent samples t-test was then used.

[0125] V. a P This is due to the group effect. b P For time effect ， c P This is the interaction effect between group and time.

[0126] VI. For different visit sites within the same intervention group, Tukey's multiple comparison test was used: compared to week 0, p < 0.01, p < 0.0001.

[0127] 4. Effects of plant extract powder intervention on patients' ESS scores after 2 and 4 weeks. Repeated measures ANOVA with Greenhouse-Geisser correction was used to conduct an overall analysis of the ESS scores of 113 subjects (placebo group n=56, plant extract powder group n=57) at three visit sites in weeks 0, 2, and 4. The results showed a main effect of group ( a P <0.0001), time main effect ( b P =0.02) and the interaction effect between group and time ( c P Statistically significant differences were observed between the two interventions (<0.0001), indicating an overall inter-group difference in the improvement of daytime sleepiness scores between the two interventions. Furthermore, both groups showed significant changes in ESS scores with prolonged intervention time. An interaction between group and time was observed, suggesting that the extent of improvement in daytime sleepiness reduction from the two interventions significantly varied with the duration of treatment. Tukey multiple comparisons within the groups showed that the placebo group had a significantly lower ESS score at week 2 compared to baseline (<0.0001). p < 0.01; the ESS scores of the plant extract powder group were significantly lower than baseline at weeks 2 and 4 after intervention (p < 0.01). (p < 0.0001) indicates that both interventions can lower ESS scores. The interaction effect further suggests that the effect of plant extract powder in improving daytime sleepiness increases with the duration of intervention and is significantly better than placebo.

[0128] A comparison of the two intervention methods at different visit points was conducted between groups. Table 9 shows the comparison of the total ESS scores of the two groups at different time points. It can be seen that at baseline in week 0, the ESS scores of the two groups were 12.02±4.01 and 13.07±3.99, respectively, with no statistically significant difference between groups (p=0.486). Figure 18 It was observed that the baseline ESS scores of the two groups were basically consistent, and the baseline daytime sleepiness of the subjects was comparable. At week 2 of the intervention, the ESS score in the placebo group was 8 (6, 12.25), and in the plant extract powder group it was 10 (6, 12), with no statistically significant difference between the groups (p=0.999). After week 4 of the intervention, the ESS score in the placebo group was 10.48±5.80, and in the plant extract powder group it was 6 (3, 8.25), with a highly significant difference between the groups. #### (p < 0.0001) Compared to the placebo group, the plant extract powder group showed a 43.82% decrease in ESS sleepiness score, with a more significant reduction in daytime sleepiness. The differences in ESS scores between the two interventions were compared between the groups at two time points: The Mann-Whitney U rank-sum test was used to compare the differences at 0-2 weeks. The median difference in the placebo group was -2.5 (-6.25, 0), while the median difference in the plant extract powder group was [missing value]. The mean difference between the groups was 3.80 ± 4.88 (p = 0.284). An independent samples t-test was used to assess the difference between weeks 0 and 4. The mean difference in the placebo group was [value missing]. 1.54±5.65, the average difference between the plant extract powder groups was The mean ESS score was 6.98 ± 5.94, indicating a highly statistically significant difference between groups (p = 0.001). The ESS score in the plant extract powder group decreased by 353.25% compared to the placebo group during weeks 0-4. The intergroup comparison of the score difference at the week 4 visit with that from weeks 0-4 further demonstrates that the plant extract powder of this invention is significantly more effective than the placebo in reducing ESS scores and improving daytime sleepiness symptoms.

[0129] Summary Table 9 and Figure 18 It can be seen that although both the placebo and the plant extract powder of the present invention can lower the subject's ESS score and improve daytime sleepiness after 4 weeks of intervention, the plant extract powder's advantage in alleviating daytime sleepiness continues to increase with the extension of intervention time, and its overall efficacy in improving daytime sleepiness is significantly stronger than that of the placebo.

[0130] Table 9

[0131] I. The normality test shows that it does not conform to a normal distribution. The Mann-Whiteny U rank-sum test is used, and the result is described using M(P25, P75).

[0132] II. The normality test (Shapiro Wilk test) shows that it conforms to a normal distribution, described using (Mean ± SD).

[0133] III. The differences between the different intervention groups at weeks 0, 2, and 4 were analyzed using the Šidák test, and the marginal mean of LS was analyzed using the t-test.

[0134] IV. The difference between different intervention groups (0-2 weeks) did not conform to the normal distribution in the Shapiro Wilk test (p < 0.05), so the Mann-Whiteny U rank-sum test was used.

[0135] V. The differences between the different intervention groups (0-4 weeks) showed p>0.05 in the Shapiro-Wilk test, indicating a normal distribution. An independent samples t-test was then used.

[0136] VI. a P This is due to the group effect. b P For time effect ， c P This is the interaction effect between group and time.

[0137] VII. For different visitation points within the same intervention group, Tukey's multiple comparison test was used: compared to week 0, p < 0.01, p < 0.0001.

[0138] 5. Effects of plant extract powder intervention on patients' GAD-7 scores after 2 and 4 weeks. A Greenhouse-Geisser corrected repeated measures ANOVA was used to analyze the GAD-7 anxiety scores of 113 subjects (n=56 in the placebo group and n=57 in the plant extract powder group) at three visit sites in weeks 0, 2, and 4. The results showed a main group effect. a P <0.0001), time main effect ( b P <0.0001) and the interaction effect between group and time ( c PThe statistical differences were all <0.0001, indicating an overall inter-group difference in the improvement of GAD-7 scores between the two interventions. Furthermore, both groups showed a significant decrease in GAD-7 scores with prolonged intervention time. An interaction between group and time was observed, indicating that the degree of anxiety relief improvement from the two interventions differentiated significantly with prolonged treatment duration. Tukey's multiple comparisons within the groups showed that the placebo group had significantly lower GAD-7 scores from baseline at weeks 2 and 4 of the intervention (<0.0001). p < 0.05; the GAD-7 scores of the plant extract powder group were significantly lower than baseline at weeks 2 and 4 after intervention (p < 0.05). (p < 0.0001) indicates that both interventions can lower GAD-7 scores. The interaction effect further suggests that the effect of plant extract powder in relieving anxiety increases with the duration of intervention and is significantly better than placebo.

[0139] A comparison of the two intervention methods at different visit points was conducted between groups. Table 10 shows the comparison of the total GAD-7 scores of the two groups at different time points. At baseline in week 0, the GAD-7 scores of the two groups were 8 (6.75, 11.25) and 9 (7, 12), respectively, with no statistically significant difference between groups (p=0.941). Figure 19 It can be seen that the baseline GAD-7 score distributions of the two groups were basically consistent, and the baseline anxiety levels of the subjects were comparable. At week 2 of the intervention, the GAD-7 score of the placebo group was 5.5 (3, 8), and that of the plant extract powder group was 5 (3, 7), with no statistically significant difference between the groups (p=0.063). After week 4 of the intervention, the GAD-7 score of the placebo group was 3 (-4.25, 0), and that of the plant extract powder group was 3 (-6, -1), with a highly significant difference between the groups. #### (p < 0.0001) The anxiety relief effect was more significant. The Mann-Whitney U rank-sum test was used to compare the differences in GAD-7 scores between the two interventions at both the 0-2 week and 0-4 week timeframes: The median difference at 0-2 week was 7 (3, 9) in the placebo group and 2 (0, 5) in the plant extract powder group, with no statistically significant difference between the groups (p = 0.056); the median difference at 0-4 week was -2.5 (-5, 1.25) in the placebo group and [missing value] in the plant extract powder group. The difference between the groups was 6.07±3.76, which was statistically significant (p<0.001). The GAD-7 score in the plant extract powder group decreased by 142.80% compared with the placebo group during the 0-4 week period. The intergroup comparison results of the week 4 visit and the score difference between the 0-4 week period together indicate that the plant extract powder of this invention is significantly better than the placebo in reducing GAD-7 scores and improving anxiety.

[0140] Combined with Table 10 Figure 19The results showed that although both the placebo and the plant extract powder of the present invention could lower the subjects' GAD-7 scores and reduce anxiety levels after 4 weeks of intervention, the plant extract powder showed a greater advantage in relieving anxiety as the intervention time increased, and its overall efficacy in improving anxiety was significantly stronger than that of the placebo.

[0141] Table 10

[0142] I. The normality test shows that it does not conform to a normal distribution. The Mann-Whiteny U rank-sum test is used, and the result is described using M(P25, P75).

[0143] II. The normality test (Shapiro Wilk test) shows that it conforms to a normal distribution, described using (Mean ± SD).

[0144] III. The differences between the different intervention groups at weeks 0, 2, and 4 were analyzed using the Šidák test, and the marginal mean of LS was analyzed using the t-test.

[0145] IV. The differences between the different intervention groups (0-2, 0-4 weeks) did not conform to the normal distribution in the Shapiro Wilk test (p < 0.05), so the Mann-Whiteny U rank-sum test was used.

[0146] V. a P This is due to the group effect. b P For time effect ， c P This is the interaction effect between group and time.

[0147] VI. For different visit sites within the same intervention group, Tukey's multiple comparison test was used: compared to week 0, p < 0.05 p < 0.0001.

[0148] 6. Effects of plant extract powder intervention on patients' PHQ-9 scores after 2 and 4 weeks. Repeated measures ANOVA with Greenhouse-Geisser correction was used to analyze the PHQ-9 depression scores of 113 subjects (n=56 in the placebo group and n=57 in the plant extract powder group) at three visit sites in weeks 0, 2, and 4. The results showed a main effect of group ( a P <0.0001), time main effect ( b P <0.0001) and the interaction effect between group and time ( cP The difference was statistically significant (<0.0001), indicating an overall inter-group difference in the improvement of PHQ-9 scores for depression between the two interventions. Furthermore, both groups showed significant changes in PHQ-9 scores with prolonged intervention time. An interaction between group and time was observed, suggesting that the degree of improvement in depressive mood from the two interventions significantly differentiated with prolonged use. Tukey multiple comparisons within the groups showed no significant difference in PHQ-9 scores from baseline at weeks 2 and 4 of the placebo group; however, the PHQ-9 scores in the plant extract powder group were significantly lower than baseline at weeks 2 and 4 of the intervention (<0.0001). (p < 0.0001) indicates that only plant extract powder can significantly downregulate the PHQ-9 depression score. The interaction effect further suggests that the effect of plant extract powder in improving depressive mood increases with the duration of intervention and is significantly better than placebo.

[0149] A comparison of the two intervention methods at different visit points was conducted between groups. Table 11 shows the comparison of the total PHQ-9 scores of the two groups at different time points. It can be seen that at baseline in week 0, the PHQ-9 scores of the two groups were 8 (7, 11.25) and 9 (7, 12), respectively, with no statistically significant difference between groups (p=0.953). Figure 20 It was observed that the baseline PHQ-9 scores of the two groups were basically consistent, and the baseline depression levels of the subjects were comparable. At week 2 of the intervention, the PHQ-9 score in the placebo group was 7.30±5.19, while that in the plant extract powder group was 5 (3, 8), with a statistically significant difference between the groups (p=0.024). After week 4 of the intervention, the PHQ-9 score in the placebo group was 8 (4.75, 10.25), while that in the plant extract powder group was 2 (0, 4), with a highly significant difference between the groups. #### (p < 0.0001) Compared to the placebo group, the plant extract powder group showed a 75.00% decrease in PHQ-9 depression scores, demonstrating a significant effect in alleviating depressive symptoms. Independent samples t-tests were used to compare the differences in PHQ-9 scores between the two interventions at two time points: 0-2 weeks: mean difference in placebo group was [value missing]. The mean difference between the plant extract powder groups was 1.61 ± 5.46. 3.96±3.64, the difference between groups was statistically significant (p=0.008); Week 0-4 difference: the mean difference in the placebo group was 0.57±5.59, the average difference among the plant extract powder groups was The difference between groups was 6.67±4.15, which was statistically significant (p<0.001). The PHQ-9 score in the plant extract powder group at weeks 0-4 was nearly 10 times lower than that in the placebo group. The intergroup comparison results of the visit points at weeks 2 and 4 with the score differences at weeks 0-2 and 0-4 together indicate that the plant extract powder of this invention is significantly more effective than the placebo in reducing the PHQ-9 depression score and improving depressive mood.

[0150] Combined with Table 11 Figure 20 The results showed that the placebo intervention for 4 weeks failed to effectively lower the PHQ-9 scores of the subjects or improve their depressive state, while the plant extract powder intervention of this invention could significantly reduce the depression score, and the improvement advantage in alleviating depression continued to increase with the extension of intervention time. The overall efficacy in improving depressive mood was significantly stronger than that of the placebo.

[0151] Table 11

[0152] I. The normality test shows that it does not conform to a normal distribution. The Mann-Whiteny U rank-sum test is used, and the result is described using M(P25, P75).

[0153] II. The normality test (Shapiro Wilk test) shows that it conforms to a normal distribution, described using (Mean ± SD).

[0154] III. The differences between the different intervention groups at weeks 0, 2, and 4 were analyzed using the Šidák test, and the marginal mean of LS was analyzed using the t-test.

[0155] IV. The differences between the different intervention groups (0-2 weeks, 0-4 weeks) showed p > 0.05 in the Shapiro-Wilk test, indicating a normal distribution. An independent samples t-test was then used.

[0156] V. aP represents the group effect, bP represents the time effect, and cP represents the interaction effect between group and time.

[0157] VI. For different visit sites within the same intervention group, Tukey's multiple comparison test was used: compared to week 0, p < 0.0001.

[0158] 7. Safety analysis of plant extract powder Blood component analysis was performed on participants before the start of the study and 4 weeks after administration. The placebo group (n=56) and the plant extract powder group (n=57) were included in the safety analysis. Before and after treatment, liver function (ALT, AST), kidney function (CREA), and complete blood count (WBC, RBC, HGB, PLT) were all within the normal range in both groups, with no significant differences. This indicates that the plant extract powder intervention had no significant effect on the patients' blood components. Table 12 shows the blood component indicators of the placebo group at different time points, and Table 13 shows the blood component indicators of the plant extract powder group at different time points.

[0159] No side effects or adverse events were recorded during the study, indicating that patients tolerated the daily use of 3g of plant extract powder well.

[0160] Table 12

[0161] Table 13

[0162] The difference before and after the intervention was normalized by the Shapiro-Wilk test and was found to be normally distributed; paired t-tests were used and the results were described using (Mean ± SD).

[0163] The embodiments provided above are not intended to limit the scope of the invention, nor are the described steps intended to limit the order of execution. Any obvious modifications made to the invention by those skilled in the art based on existing common knowledge also fall within the scope of protection defined by the claims.

Claims

1. A functional food having effects of improving insomnia and anxiety, comprising, The composition of each raw material, by weight, is as follows: 5-12 parts of Ganoderma lucidum extract 5-15 parts of tanshinone extract 5-15 parts of Astragalus extract Jujube extract 3-15 parts Anemarrhena asphodeloides extract 3-12 parts Cyperus rotundus extract 2-10 parts; All raw materials are solid powders derived from water extracts.

2. The functional food according to claim 1, characterized in that, The composition of each raw material, by weight, is as follows: 5.8 parts of Ganoderma lucidum extract 5.3 parts of tanshinone extract Astragalus extract 5.0 parts Jujube extract 3.3 parts Anemarrhena asphodeloides extract 3.3 parts Cyperus rotundus extract 2.5 parts.

3. The functional food according to claim 1, wherein the content of Ganoderma lucidum polysaccharides in the Ganoderma lucidum extract is ≥10%, and the content of total triterpenes and sterols is ≥5%; the content of tanshinone IIA in the Salvia miltiorrhiza extract is ≥1.0%; the content of astragaloside IV in the Astragalus membranaceus extract is ≥0.5%; the content of jujube polysaccharides in the jujube extract is ≥15%; the content of anemarrhena saponin BII in the Anemarrhena asphodeloides extract is ≥8%; and the content of α-cyperone in the Cyperus rotundus extract is ≥1.0%.

4. The functional food according to claim 1, characterized in that, Dosage forms include granules, tablets, capsules, powders, granules, or blister packs.

5. The functional food according to claim 1, characterized in that, Functional foods include health foods.

6. The functional food according to claim 1, characterized in that, Functional foods also include acceptable food additives.

7. The functional food according to claim 8, characterized in that, The excipients include maltodextrin and steviol glycosides.

8. The application of a functional food according to any one of claims 1-7, characterized in that, Used to prepare health food products that can improve insomnia and anxiety.

9. A method for preparing the functional food according to claim 1, characterized in that, The functional food is in granule form and includes the following steps: (1) Mix 5-12 parts of Ganoderma lucidum extract, 5-15 parts of Salvia miltiorrhiza extract, 5-15 parts of Astragalus membranaceus extract, 3-15 parts of jujube extract, 3-12 parts of Anemarrhena asphodeloides extract and 2-10 parts of Cyperus rotundus extract evenly to obtain a raw material mixture. (2) Add 0-10 parts of maltodextrin and 0-0.2 parts of steviol glycosides to the raw material mixture and mix thoroughly to obtain a soft material; (3) The soft material is granulated, dried and sized at a temperature below 60°C to obtain the granule product.

10. A method for preparing the functional food according to claim 1, characterized in that, The functional food is in capsule form and includes the following steps: (1) Mix 5-12 parts of Ganoderma lucidum extract, 5-15 parts of Salvia miltiorrhiza extract, 5-15 parts of Astragalus membranaceus extract, 3-15 parts of jujube extract, 3-12 parts of Anemarrhena asphodeloides extract and 2-10 parts of Cyperus rotundus extract evenly to obtain a raw material mixture. (2) Place the raw material mixture together with 0-10 parts of maltodextrin and 0-0.2 parts of steviol glycosides in a mixer and pulverize and mix thoroughly to obtain a uniform dry powder mixture; (3) The dry powder mixture is filled into a capsule shell to obtain the capsule product.

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