Use of safflower honey, or safflower honey extract, in increasing adh and aldh activity

Abstract

This invention relates to the field of functional food technology, and more particularly to the application of safflower honey, or safflower honey extract, in enhancing the activity of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH). The invention has found that safflower honey, or safflower honey extract, can effectively enhance ADH and ALDH activity, thereby promoting alcohol metabolism and achieving a hangover-relieving effect. Further research on the extract revealed that a mixture of syringaldehyde, riboflavin, lutein, luciferin, and three p-coumaroyl spermidine plays a key role in enhancing ADH and ALDH activity, thus providing an application of this mixture in hangover relief. The application of safflower honey and its extract provided by this invention has high application value for developing foods and health products with hangover-relieving effects.

Description

Technical Field

[0001] This invention relates to the field of functional food technology, and more particularly to the application of safflower honey, or safflower honey extract, in enhancing ADH and ALDH activity. Background Technology

[0002] Honey is a natural sweetener produced by bees from nectar, secretions from living plants, or excrement from insects feeding on living plants. It is obtained by bees collecting nectar, mixing it with their own unique substances, and then transforming, depositing, dehydrating, storing, and preserving it in the honeycomb until it matures. As a natural sweetener, honey is not only rich in nutrients, but also contains different bioactive plant compounds depending on the nectar source plant, giving it unique functions. This makes research on the efficacy of specific honey varieties uncertain. Safflower honey, for example, is made from safflower (Carthamus tinctorius L.), which has a distinctive aroma and a slightly bitter taste. It possesses certain medicinal value and is used for amenorrhea, dysmenorrhea, lochia retention, abdominal masses, chest pain, abdominal pain due to blood stasis, chest and rib pain, injuries from falls, and sores and swellings. It has the effects of promoting blood circulation, relieving pain, and dispersing blood stasis. It also softens blood vessels, promotes blood circulation, and regulates endocrine disorders.

[0003] Alcohol culture has a long history and is an indispensable element of food culture. Long-term excessive drinking can cause significant harm to the body, leading to health problems such as liver damage, cardiovascular disease, and impaired immune system. Furthermore, acute heavy drinking can cause intoxication symptoms, triggering various subsequent behaviors that seriously threaten life and property. The symptoms of intoxication are closely related to the concentration of alcohol (ethanol) in the blood. Modern research shows that the main route of ethanol absorption after drinking is through the gastrointestinal tract, with approximately 25% absorbed by the stomach and 75% by the intestines. After absorption and digestion in the gastrointestinal tract, ethanol is primarily metabolized in the liver. As the main organ and site of ethanol metabolism, the activities of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) in the liver are closely related to ethanol metabolism. According to the metabolic mechanism of ethanol in the human body, ethanol is first oxidized to acetaldehyde in the liver by ADH. If the metabolic rate of ethanol in the liver is much lower than its absorption rate, it will act on the brain, causing central nervous system disorders. Acetaldehyde is then oxidized to acetic acid by ALDH. Excessive accumulation of toxic acetaldehyde in the body can cause discomfort such as facial flushing, headache, and vomiting, potentially damaging internal organs. Finally, acetic acid is oxidized through the tricarboxylic acid cycle, ultimately producing water and carbon dioxide, which are then excreted from the body. Therefore, the ability to effectively promote and enhance the activity of ADH and ALDH is an important indicator for evaluating the efficacy of hangover remedies. Summary of the Invention

[0004] To address the problems existing in the prior art, the present invention provides the application of safflower honey, or safflower honey extract, in enhancing ADH and ALDH activity.

[0005] With increasing health awareness, the demand for hangover remedies made from natural raw materials to reduce the negative effects of alcohol consumption is growing. This invention, through research, has discovered that safflower honey enhances ADH and ALDH activity, with a significantly superior effect compared to other types of honey. Further research into its components has led to this discovery. Honey contains a wide variety of complex compounds, which are easily influenced by the nectar source. This invention, through extensive research and analysis, has yielded a composition that promotes alcohol metabolism and exhibits excellent hangover-relieving effects. Furthermore, these natural bioactive components have no side effects and are easily accepted by the public, making the resulting hangover remedy product significant and promising for future applications.

[0006] In a first aspect, the present invention provides a hangover relief composition, comprising:

[0007] Syringaldehyde, riboflavin, lutein, lutein and three-p-coumaroyl spermidine.

[0008] Further, by weight, it includes:

[0009] Syringaldehyde 22-93 parts, riboflavin 1-6 parts, lutein 14-54 parts, lutein 15-70 parts, and triscoumaryl spermidine 1-9 parts.

[0010] Furthermore, it also includes one or more of p-hydroxybenzoic acid, p-hydroxybenzaldehyde, or p-coumaric acid.

[0011] Secondly, the present invention provides the use of any one or more components of the hangover relief composition, or safflower honey, or safflower honey extract, in promoting alcohol metabolism.

[0012] The present invention further provides the use of any one or more components of the hangover relief composition, or safflower honey, or safflower honey extract, in enhancing ADH and ALDH activity.

[0013] Furthermore, the safflower honey extract is prepared by the following method:

[0014] Solid-phase extraction was used to enrich polyphenolic compounds in safflower honey.

[0015] Furthermore, the safflower honey extract is prepared by the following method:

[0016] Dissolve safflower honey in water and adjust the pH to 6.5–7.5; centrifuge to remove solid impurities and collect the supernatant; use the supernatant for solid-phase extraction, using methanol or a methanol solution containing formic acid as the eluent.

[0017] Existing technologies generally consider the hangover-relieving effect of honey to be due to the natural sugars it contains, such as glucose and fructose. However, those skilled in the art will understand that the safflower honey extract obtained based on the preparation method provided by this invention includes the aforementioned components such as syringaldehyde, riboflavin, lutein, luciferin, and triscoumaryl spermidine, but does not include natural sugars such as glucose and fructose. Therefore, its ability to promote alcohol metabolism is something that is difficult to conceive of in the prior art.

[0018] Thirdly, the present invention provides a hangover relief product, which includes the aforementioned hangover relief composition; the hangover relief product is a food, health product, or drug.

[0019] Furthermore, the concentration of eugenol in the hangover relief product is above 0.5 mg / mL.

[0020] Furthermore, the concentration of riboflavin in the hangover relief product is above 0.05 mg / mL, the concentration of lutein is above 0.5 mg / mL, the concentration of lutein is above 0.5 mg / mL, and the concentration of triscoumaside is above 0.05 mg / mL.

[0021] Furthermore, the concentration of eugenol in the hangover relief product is 1-3 mg / mL, the concentration of riboflavin is 0.1-0.3 mg / mL, the concentration of lutein is 1-3 mg / mL, the concentration of photopigment is 1-3 mg / mL, and the concentration of triscoumaside is 0.1-0.3 mg / mL.

[0022] This invention provides preferred concentrations of active substances in a hangover remedy, at which its effect on promoting alcohol metabolism exceeds that of safflower honey extract itself. This further illustrates the contribution of the hangover remedy composition discovered in this invention to promoting alcohol metabolism.

[0023] Fourthly, the present invention provides a hangover relief product, the hangover relief product comprising safflower honey extract;

[0024] The safflower honey extract was prepared by the following method:

[0025] Solid-phase extraction was used to enrich polyphenolic compounds in safflower honey.

[0026] Furthermore, the safflower honey extract is prepared by the following method:

[0027] Dissolve safflower honey in water and adjust the pH to 6.5–7.5; centrifuge to remove solid impurities and collect the supernatant; use the supernatant for solid-phase extraction, using methanol or a methanol solution containing formic acid as the eluent.

[0028] Furthermore, the elution was performed in two stages: the first stage used methanol, and the second stage used a methanol solution containing formic acid.

[0029] Furthermore, the formic acid content in the methanol solution containing formic acid is 3-10%.

[0030] The present invention has the following effects:

[0031] This invention has discovered that safflower honey can increase the activity of ADH and ALDH, thereby promoting alcohol metabolism and achieving a hangover-relieving effect. Further research on its extract yielded a composition that effectively promotes ADH and ALDH activity. This composition can effectively promote alcohol metabolism, which is of great significance and application value for the development of hangover-relieving products. Attached Figure Description

[0032] To more clearly illustrate the technical solutions in this invention or the prior art, the drawings used in the description of the embodiments or the prior art will be briefly introduced below. Obviously, the drawings described below are some embodiments of this invention. For those skilled in the art, other drawings can be obtained from these drawings without creative effort.

[0033] Figure 1 This is the HPLC chromatogram of safflower honey provided in Example 1 of the present invention.

[0034] Figure 2 This is a comparative diagram showing the ability of safflower honey, acacia honey, linden honey, vitex honey, and rapeseed honey to activate ADH and ALDH activity, provided in Embodiment 2 of the present invention.

[0035] Figure 3 This is a schematic diagram comparing the ability of different groups of honey extracts to activate ADH and ALDH activity, provided in Example 3 of the present invention. Detailed Implementation

[0036] To make the objectives, technical solutions, and advantages of this invention clearer, the technical solutions of this invention will be clearly and completely described below with reference to the accompanying drawings. Obviously, the described embodiments are only some, not all, of the embodiments of this invention. All other embodiments obtained by those skilled in the art based on the embodiments of this invention without creative effort are within the scope of protection of this invention.

[0037] Example 1

[0038] This embodiment is based on the HPLC chromatogram of safflower honey (e.g., Figure 1 As shown in the figure, the composition and content of the collected safflower honey were determined.

[0039] The specific operating method is as follows:

[0040] 1. Accurately weigh 20g of safflower honey sample, add 80mL of ultrapure water, stir thoroughly to dissolve, and then adjust the pH to about 7 with diluted ammonia.

[0041] 2. The sample solution was centrifuged at 8500×g for 20 min to remove solid impurities, and the supernatant was then collected for later use.

[0042] 3. Activate the Strata-XA solid-phase extraction column with 4 mL of analytical grade methanol, and then add 4 mL of ultrapure water for equilibration;

[0043] 4. Add the supernatant to the solid-phase extraction column to enrich polyphenolic compounds. After the supernatant has passed through the solid-phase extraction column, rinse the column with 4 mL of ultrapure water to ensure that all residual solution adhering to the column passes through. Then elute the solid-phase extraction column with 1 mL of chromatographic grade methanol and collect the eluent. Perform a second elution with 2 mL of methanol solution containing 5% formic acid and collect the eluent.

[0044] 5. All eluent was dried under nitrogen blowing, then reconstituted with 2 mL of a reconstituted solution containing 2% chromatographic grade acetic acid, 23% ultrapure water, and 75% chromatographic grade methanol. Finally, it was filtered through a 0.22 μm filter membrane for high performance liquid chromatography analysis.

[0045] 6. The high-performance liquid chromatography (HPLC) method is as follows: mobile phase A is water (containing 0.2% acetic acid), and mobile phase B is methanol (containing 0.2% acetic acid). The chromatographic column is C10. 18 (150×4.6mm, 5μm); UV detection wavelength 270nm, sample volume 20μL, total flow rate 0.7mL / min. The liquid chromatography elution program was as follows:

[0046] 0-11 min, 9-15% B;

[0047] 11-18 min, 15% B;

[0048] 18-28 min, 15-17% B;

[0049] 28-30 min, 17-22% B;

[0050] 30-39 min, 22-26% B;

[0051] 39-46 min, 26-32% B;

[0052] 46-56 min, 32-33% B;

[0053] 56-60 min, 33-34% B;

[0054] 60-70 min, 34-37% B;

[0055] 70-80 min, 37-41% B;

[0056] 80-90 min, 41-45% B;

[0057] 90-100 min, 45-51% B;

[0058] 100-105 min, 51-54% B;

[0059] 105-110 min, 54-57% B;

[0060] 110-120 min, 57-64% B;

[0061] 120-130 min, 64-70% B;

[0062] 130-135 min, 70-80% B.

[0063] 7. Calculate the contents of eugenol, p-hydroxybenzoic acid, p-hydroxybenzaldehyde, p-coumaric acid, riboflavin, lutein, lutein, and triscoumaryl spermidine using the external standard method.

[0064] In this embodiment, six different safflower honey samples were tested using the method described above, and they were numbered C01-C06 respectively (sample collection information is shown in Table 1).

[0065] Table 1. Information on Safflower Honey Sample Collection

[0066] Sample number Sample Name Collection site C01 Safflower honey (Carthamus tinctorius L.) Xinjiang C02 Safflower honey (Carthamus tinctorius L.) Xinjiang C03 Safflower honey (Carthamus tinctorius L.) Xinjiang C04 Safflower honey (Carthamus tinctorius L.) Xinjiang C05 Safflower honey (Carthamus tinctorius L.) Xinjiang C06 Safflower honey (Carthamus tinctorius L.) Xinjiang

[0067] The specific results of the content tests for eugenol, p-hydroxybenzoic acid, p-hydroxybenzaldehyde, p-coumaric acid, riboflavin, lutein, luciferin, and tri-coumaroyl spermidine are shown in Table 2.

[0068] Table 2. Plant compound content (mg / kg) in safflower honey samples

[0069]

[0070]

[0071] Example 2

[0072] This embodiment investigated the in vitro activation abilities of safflower honey, acacia honey, linden honey, vitex honey, and rapeseed honey on ADH and ALDH, using the following steps:

[0073] 1. ADH activity was detected using the Valle & Hoch method with slight modifications. Specifically, 1.5 mL of 0.1 mol / L sodium pyrophosphate buffer (pH = 8.8) and 1.0 mL of 27 mmol / L oxidized coenzyme I (NAD) were added. + The following solutions were prepared: 0.5 mL of 11.5% (v:v) ethanol solution and 0.1 mL of 1.0 g / mL aqueous solution of safflower honey (sample CO5), acacia honey, linden honey, vitex honey, or rapeseed honey. The mixture was thoroughly mixed and incubated in a water bath at 25°C for 5 min. Immediately afterward, 0.1 mL of LADH (0.25 U / mL) solution was added and the mixture was shaken well. The control group consisted of 0.1 mL of distilled aqueous solution, with all other procedures performed identically. After shaking, the absorbance was measured at 340 nm using a spectrophotometer, with readings taken every 30 s for 5 min. The absorbance (A) was plotted against time, and A was calculated. 340 The ADH activity was calculated based on the increase in the number of nanomoles of NADH generated per minute, using the molar extinction coefficient of the generated reduced coenzyme I (NADH) at 340 nm as 6.22. The ADH activity was expressed as the number of nanomoles of NADH generated per minute. All the methods used for measuring these indicators employed conventional methods well-known in the art.

[0074]

[0075]

[0076] 2. ALDH activity was detected using the Blair & Bodley method with slight modifications. Specifically, 1.6 mL of 0.1 mol / L sodium pyrophosphate buffer (pH = 9.5) and 1.0 mL of 3.6 mmol / L oxidized coenzyme I (NAD) were added. + The following solutions were prepared: 0.1 mL of 0.1 mol / L acetaldehyde solution, 0.1 mL of 10 mmol / L pyrazole solution, and 0.1 mL of 1.0 g / mL aqueous solution of safflower honey (sample CO5), acacia honey, linden honey, vitex honey, or rapeseed honey. The mixture was thoroughly mixed and incubated in a 30°C water bath for 5 min. Immediately afterward, 0.1 mL of ALDH (0.25 U / mL) solution was added and the mixture was shaken well. The control group consisted of 0.1 mL of distilled aqueous solution, with all other procedures performed identically. After shaking, the absorbance at 340 nm was measured using a spectrophotometer, with readings taken every 1 min until the increase in absorbance per minute stabilized. The absorbance (A) was plotted against time, and A was calculated. 340The ALDH activity was calculated based on the increase in ALDH per minute, using the molar extinction coefficient of the generated reduced coenzyme I (NADH) at 340 nm as 6.22. ALDH activity was expressed as the number of nanomoles of NADH generated per minute. All the methods used for measuring these indicators employed conventional methods well-known in the art.

[0077]

[0078]

[0079] For details, please see [link / details]. Figure 2 The results showed that safflower honey, acacia honey, linden honey, vitex honey, and rapeseed honey all possessed a certain ability to activate ADH and ALDH activity. Among the five types of honey, safflower honey exhibited higher activation rates for both ADH and ALDH than the other honeys, reaching 16.33% and 14.46%, respectively. The order of their activation ability was: safflower honey > linden honey > acacia honey > vitex honey > rapeseed honey.

[0080] Example 3

[0081] This embodiment evaluates the in vitro activation ability of honey extracts from safflower honey, acacia honey, linden honey, vitex honey, and rapeseed honey to activate ADH and ALDH.

[0082] The honey extract solutions were prepared by processing safflower honey (samples CO4, CO5, and CO6), acacia honey, linden honey, vitex honey, and rapeseed honey according to steps ①-④ of Example 1. The resulting eluents were dried under nitrogen and then dissolved in 2 mL of sodium pyrophosphate buffer containing 1% DMSO. Then, the effects of the honey extract solutions of safflower honey, acacia honey, linden honey, vitex honey, and rapeseed honey on in vitro ADH and ALDH activities were detected using the method described in Example 2.

[0083] For details, please see [link / details]. Figure 3 The results showed that the activation rates of ADH and ALDH by safflower honey extracts (samples CO4, CO5, and CO6) were higher than those by other honey extracts. Furthermore, compared to honey, the activation effects of safflower honey extract on ADH and ALDH were significantly more pronounced. The activation rates of ADH and ALDH by samples CO4, CO5, and CO6 were 30.12%, 32.22%, and 34.33%, and 24.78%, 26.75%, and 27.56%, respectively. In addition, the activation rates of ADH and ALDH showed a positive correlation with the contents of syringaldehyde, 4-hydroxybenzoic acid, p-hydroxybenzaldehyde, p-coumaric acid, riboflavin, lutein, luciferin, and tris(p-coumaryl)semidine in the safflower honey extract. This indicates that safflower honey extract has a good activation ability for ADH and ALDH.

[0084] Example 4

[0085] This embodiment evaluates the ability of safflower honey to activate ADH and ALDH in vivo.

[0086] Specifically, an acute alcohol poisoning mouse model was established to evaluate the effects of safflower honey on ADH and ALDH activities in mouse liver. Fifty Kunming mice, weighing 20±2g, were randomly divided into five groups (n=10 each) after one week of acclimatization: a normal control group, a model group, a low-dose experimental group, a medium-dose experimental group, and a high-dose experimental group. For the first gavage, the normal control and model groups received saline, while the low-dose experimental group received safflower honey (sample C05) at 5g / kg bw, the medium-dose group at 15g / kg bw, and the high-dose group at 30g / kg bw. A second gavage was administered 40 minutes later. For the second gavage, the normal control group received 12mL / kg bw saline, while the other groups received 12mL / kg bw baijiu (a type of Chinese liquor). Forty minutes after gavage, the mice were euthanized by dislocation, and their livers were immediately dissected and removed on ice. Accurately weigh 0.1g of liver tissue, add pre-cooled physiological saline, and homogenize using a homogenizer under ice bath conditions. Centrifuge the homogenate at 2500 rpm for 15 min at 4°C, collect the supernatant, and store it at -80°C for later testing. Detect ADH and ALDH activities according to the kit instructions. All methods described herein are standard and well-known in the art.

[0087] The specific results are shown in Table 3. The results indicated that the ADH and ALDH activities in the liver of the model group mice were significantly increased compared to the normal control group (P < 0.05), indicating that ADH and ALDH activities in the mouse liver increased after alcohol consumption. Compared with their respective model groups, the low-dose, medium-dose, and high-dose experimental groups all showed further increases in ADH and ALDH activities. Among them, the medium-dose and high-dose experimental groups showed significant differences compared to the model group (P < 0.05). This indicates that gavage administration of safflower honey can enhance the ADH and ALDH activities in the mouse liver, and the increase in activity is positively correlated with the dosage of safflower honey.

[0088] Table 3. Effects of safflower honey on liver ADH and ALDH activity in mice with acute alcohol poisoning.

[0089] Grouping ADH / (U / mg prot) ALDH / (U / mg prot) normal control group 15.88±1.62 12.27±1.56 Model group <![CDATA[20.66±1.85 # ]]> <![CDATA[17.32±1.43 # ]]> Low-dose experimental group 23.48±1.76 19.42±1.68 Medium-dose experimental group 25.88±2.02* 21.48±1.87* High-dose experimental group 27.32±2.21* 23.01±1.96*

[0090] # indicates a comparison with the normal control group, P < 0.05; * indicates a comparison with the model group, P < 0.05.

[0091] Example 5

[0092] This embodiment evaluated the in vivo activation abilities of safflower honey extract and a mixture of eugenol, riboflavin, lutein, luciferin, and tricoumaryl spermidine, as well as the effects of these substances on ADH and ALDH activity in mouse liver using a mouse model of acute alcohol poisoning. The procedure is as follows:

[0093] One hundred Kunming mice, weighing 20±2g, were selected and randomly divided into 10 groups after one week of acclimatization. Each group consisted of 10 mice: normal control group, model group, extract experimental group, standard dose mixture group, high dose mixture group, syringaldehyde group, riboflavin group, luteolin group, luteolin group, and three-p-coumaroyl spermidine group.

[0094] In the extract experimental group, the sample CO5 was treated in steps 1-4 of Example 1, and the eluent was dried with nitrogen and then dissolved in 2 mL of aqueous solution containing 1% DMSO (specifically, 20 g of sample CO5 was used for extraction).

[0095] The standard dose mixture consisted of 2 mL of 1% DMSO aqueous solution containing 0.5 mg / mL syringaldehyde, 0.05 mg / mL riboflavin, 0.5 mg / mL lutein, 0.5 mg / mL luciferin, and 0.05 mg / mL triscoumaryl spermidine.

[0096] The high-dose mixture consisted of 2 mL of 1% DMSO aqueous solution containing 2.0 mg / mL syringaldehyde, 0.2 mg / mL riboflavin, 2.0 mg / mL lutein, 2.0 mg / mL luciferin, and 0.2 mg / mL coumarin-spermidine.

[0097] The eugenol group, riboflavin group, luteoflavin group, lutein group, and triscoumacidin-spermidine group were each 2 mL of 1% DMSO aqueous solution containing 1.6 mg / mL of each compound.

[0098] The normal control group, model group, extract experimental group, standard dose mixture group, high dose mixture group, syringaldehyde group, riboflavin group, luteoflavin group, lutein group, and three-p-coumaroyl spermidine groups were administered 10 mL / kg bw of physiological saline, physiological saline, extract solution, standard dose mixture solution, high dose mixture solution, and each compound solution by gavage daily for 30 consecutive days. Forty minutes after the last gavage, except for the normal control group which received 12 mL / kg bw of physiological saline, all other groups received 12 mL / kg bw of baijiu (a type of Chinese liquor). Two hours after gavage, the mice in each group were euthanized by dislocation, and the livers were immediately dissected on ice. A small amount of liver tissue was taken, and 9 times the volume of physiological saline was added. The mixture was homogenized at low temperature using a homogenizer, centrifuged at 2500 r / min for 15 min at 4°C, and the supernatant was collected and stored at -80°C for later testing. ADH and ALDH activities were detected according to the kit instructions. All methods for measuring the indicators were conventional methods known in the art.

[0099] The specific results are shown in Table 4. The results indicated that, compared with the normal control group, the activities of ADH and ALDH in the liver of the model group were significantly increased (P < 0.05). Compared with the model group, the activities of ADH and ALDH in the extract experimental group, the standard dose mixture group, and the high dose mixture group were all significantly increased (P < 0.05). Among them, the standard dose mixture group and the high dose mixture group showed greater increases in ADH and ALDH activities than the extract experimental group, and the high dose mixture group showed a significant difference compared with the extract experimental group (P < 0.05), indicating that the mixture of syringaldehyde, riboflavin, lutein, luciferin, and three-coumaroyl spermidine has the ability to enhance the activity of ADH and ALDH in the liver. Furthermore, the results of the syringaldehyde group, riboflavin group, lutein group, luciferin group, and three-coumaroyl spermidine group showed that, compared with the model group, all five compounds had a certain effect on promoting the increase of ADH and ALDH activities. Among them, eugenol and tricoumaryl spermidine showed better promoting effects on ADH activity than riboflavin, lutein, and luciferin; riboflavin, lutein, and luciferin showed better promoting effects on ALDH activity than eugenol and tricoumaryl spermidine. Furthermore, the eugenol group, riboflavin group, lutein group, luciferin group, and the tricoumaryl spermidine standard dose mixture group all showed higher promoting effects on ADH and ALDH activity than the individual groupings. Therefore, eugenol, riboflavin, lutein, luciferin, and tricoumaryl spermidine enhance ADH and ALDH activity through the synergistic effect of their components.

[0100] Table 4. Effects of safflower honey extract and a mixture of eugenol, riboflavin, lutein, luciferin, and tristigrin on liver ADH and ALDH activity in mice with acute alcohol poisoning.

[0101]

[0102]

[0103] a represents the comparison with the normal control group, P < 0.05; b represents the comparison with the model group, P < 0.05.

[0104] c indicates comparison with the extract experimental group, P < 0.05

[0105] Finally, it should be noted that the above embodiments are only used to illustrate the technical solutions of the present invention, and not to limit them; although the present invention has been described in detail with reference to the foregoing embodiments, those skilled in the art should understand that modifications can still be made to the technical solutions described in the foregoing embodiments, or equivalent substitutions can be made to some of the technical features; and these modifications or substitutions do not cause the essence of the corresponding technical solutions to deviate from the spirit and scope of the technical solutions of the embodiments of the present invention.

Claims

1. A hangover remedy composition, characterized in that, By weight, it includes: Syringaldehyde 22-93 parts, riboflavin 1-6 parts, lutein 14-54 parts, lutein 15-70 parts, and triscoumaryl spermidine 1-9 parts.

2. The hangover relief composition according to claim 1, characterized in that, Also includes: p-hydroxybenzoic acid, p-hydroxybenzaldehyde or p - One or more of the following coumaric acids.

3. The use of the hangover relief composition according to claim 1 or 2 in promoting alcohol metabolism.

4. The use of the hangover relief composition according to claim 1 or 2 in enhancing ADH and ALDH activity.

5. A hangover remedy product, characterized in that, The hangover relief product includes the hangover relief composition according to any one of claims 1 or 2; the hangover relief product is a food, health product, or drug.

6. The hangover relief product according to claim 5, characterized in that, In the hangover remedy, the concentration of eugenol is above 0.5 mg / mL; and / or, the concentration of riboflavin is above 0.05 mg / mL; and / or, the concentration of lutein is above 0.5 mg / mL; and / or, the concentration of photopigment is above 0.5 mg / mL; and / or, the concentration of tricoumarin spermidine is above 0.05 mg / mL.

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