Application of astragenol in preparation of product for treating or relieving Parkinson's disease

Abstract

The invention discloses an application of astragenol in preparation of a product for treating or relieving Parkinson's disease. The behavior and pathological and pharmacological action of astragenol on PD are discussed through in-vitro and in-vivo PD models, the intervention effect of astragenol on the inflammation level is evaluated, and differential metabolites and genes are analyzed through metabonomics and transcriptomics. Enrichment pathway analysis is used for identifying intervention signal pathways and key genes, and results of omics analysis are verified. Finally, the molecular mechanism of astragenol for exerting a neuroprotective effect on neuroinflammation and PD is clarified, and a theoretical basis is provided for development of astragenol as a novel dietary supplement.

Description

Technical Field

[0001] The present invention relates to the field of biomedicine, and in particular to application of astragalool in preparing products for treating or alleviating Parkinson's disease. Background Art

[0002] Parkinson's disease (PD) is the second largest neurodegenerative disease in the world, second only to Alzheimer's disease. In recent years, the incidence of PD has increased year by year, and the age of onset has become younger and younger. Therefore, exploring treatment strategies for PD is a thorny issue around the world. At present, the clinical treatment of PD mainly involves chemical drugs such as levodopa, which are used to compensate for the decrease in dopamine concentration in the brain caused by Parkinson's disease or inhibit its degradation. However, long-term medication can easily lead to adverse reactions such as drug resistance, which hinders the improvement of symptoms in PD patients. Due to the bottleneck of PD chemical drug exploration, the research of natural products has become an important source for new drug development. Therefore, exploring new natural products and finding effective and stable potential drugs for the treatment of PD are challenging and of practical significance for PD research.

[0003] The pathogenesis of PD involves multiple pathways, including abnormal aggregation of α-synuclein, oxidative stress, mitochondrial dysfunction, neuroinflammation, etc. Neuroinflammation is a common feature of various etiologies. In recent years, many effective substances have been found in natural products and their derivatives, such as ginsenosides, berberine, piperine, etc., which have significant improvement effects on neuroinflammation and neurodegenerative diseases. Therefore, potential drugs for the treatment of neurodegenerative diseases based on neuroinflammation research have become a hot direction.

[0004] As a "medicine and food homologue", Astragalus can enhance human immunity and is widely used in the fields of food health and food hygiene. Astragaloside IV, the main active ingredient of Astragalus, has multiple pharmacological activities. Its aglycone structure cycloastragenol is the only telomerase activator from natural sources and has been successfully marketed as a dietary supplement for delaying aging. Astragalool, as an allosteric open-ring compound of cycloastragenol, is the product of acid hydrolysis of cycloastragenol. However, since the properties of the ring structure and the open-ring structure are often very different, it is not certain whether astragalool can also relieve or treat PD symptoms. For example, strychnine is a natural product with strong neurotoxicity, but the toxicity and other activities of its metabolites after ring opening are quite different, which adds activity uncertainty to the opening of the bridge ring and is a challenge for structural diversity research. Summary of the invention

[0005] The purpose of the present invention is to provide a product for treating or alleviating Parkinson's disease and application of astragalool in preparing a product for treating or alleviating Parkinson's disease.

[0006] The present invention claims to protect the use of astragalool in preparing products for treating or alleviating Parkinson's disease.

[0007] Furthermore, the product is a medicine or a health product.

[0008] Furthermore, the health care product is a dietary supplement.

[0009] Furthermore, the treatment or alleviation of Parkinson's disease is embodied in:

[0010] 1) Relieve movement disorders caused by MPTP;

[0011] 2) Reduce inflammatory factors in serum and brain tissue;

[0012] 3) Improve the abnormal aggregation of α-synuclein.

[0013] The invention provides a product for treating or alleviating Parkinson's disease. The active ingredient of the product comprises astragalool.

[0014] Furthermore, the product is a medicine or a health product.

[0015] Furthermore, the health care product is a dietary supplement.

[0016] Furthermore, the treatment or alleviation of Parkinson's disease is embodied in:

[0017] 1) Relieve movement disorders caused by MPTP;

[0018] 2) Reduce inflammatory factors in serum and brain tissue;

[0019] 3) Improve the abnormal aggregation of α-synuclein.

[0020] In the present invention, the behavioral and pathological pharmacological effects of AST on PD were explored through in vitro and in vivo PD models, its intervention effect on inflammatory levels was evaluated, and differential metabolites and genes were analyzed by metabolomics and transcriptomics. Enrichment pathway analysis was used to identify intervention signaling pathways and key genes, and the results of omics analysis were verified. Finally, the molecular mechanism of AST's neuroprotective effect on neuroinflammation and PD was elucidated, providing a theoretical basis for the development of AST as a new dietary supplement. BRIEF DESCRIPTION OF THE DRAWINGS

[0021] Figure 1 The pharmacodynamics of AST on PD in vitro and in vivo models are studied. (A) Chemical structure of AST; (BC) PD in vitro model (MPP +(D) Experimental method of MPTP-induced PD model; (EF) Gait measurement; (G) Pole climbing test; (H) Immunofluorescence staining analysis of α-synuclein. Data are expressed as mean ± SD of three independent repeated experiments ( * vs Control; # vs Model; * / # p<0.05, ** / ## p<0.01, *** / ### p<0.001).

[0022] Figure 2 AST inhibits MPTP-induced neuroinflammation. (AB) Detection of inflammatory factors in brain tissue and serum; (CE) Immunofluorescence staining analysis of TH and Iba-1 expression; (FI) Western Blot analysis of TH and Iba-1 expression. Data are expressed as mean ± SD of three independent repeated experiments. (*p<0.05, **p<0.01, ***p<0.001).

[0023] Figure 3 AST regulates the amino acid metabolism pathway. Among them, (A) PLS-DA analysis of Con and Mod and AST-H, Con and Mod, Mod and AST-G. (B) KEGG analysis related to differential metabolites. C Venn diagram of metabolite differences between groups.

[0024] Figure 4 AST can upregulate the expression of VDR gene. Among them, (AC) comparison of model with AST-H, KEGG, Go and differential gene expression; (DF) qRT-PCR verification of Cnn1, VDR and Retnlg genes; (G, H) Western Blot detection of VDR protein expression level in brain tissue. Data are expressed as mean ± standard deviation of three independent repeated experiments (*p<0.05, **p<0.01, ***p<0.001).

[0025] Figure 5 AST can reduce oxidative stress levels and inhibit ferroptosis. Among them, (A) brain tissue iron accumulation (Prussian blue staining); (BF) expression levels of ferroptosis-related proteins in brain tissue; (GI) expression levels of Nrf2 / HO-1 in brain tissue. (*p<0.05, **p<0.01, ***p<0.001).

[0026] Figure 6This is a comparison chart of the activities between cycloastragenol and astragenol. DETAILED DESCRIPTION

[0027] The present invention is further described in detail below in conjunction with specific embodiments, and the examples provided are only for illustrating the present invention, rather than for limiting the scope of the present invention. The examples provided below can be used as a guide for further improvements by those of ordinary skill in the art, and do not constitute a limitation of the present invention in any way.

[0028] The experimental methods in the following examples, unless otherwise specified, are all conventional methods, and are performed according to the techniques or conditions described in the literature in the field or according to the product instructions. The materials, reagents, etc. used in the following examples, unless otherwise specified, can all be obtained from commercial channels.

[0029] Unless otherwise specified, the quantitative tests in the following examples were performed three times and the results were averaged.

[0030] Materials and Methods

[0031] Chemical reagents and consumables. Astragalol (AST, CAS: 86541-79-9) and cycloastragalol (CAS: 78574-94-4) were purchased from Chengdu Aifa Biotechnology Co., Ltd. MPTP and MPP + Purchased from Sigma-Aldrich. CCK-8 and LDH kits were purchased from Beijing Solebaugh Technology Co., Ltd. PCR experimental consumables were purchased from Shanghai Shenggong Biological Co., Ltd. IL-1β, IL-6, TNF-α kits were purchased from Wuhan Beiyinlai Biotechnology Co., Ltd. Anti-TH, Anti-Iba-1, Anti-TfRC, Anti-FTH, Anti-Fpn, Anti-GPX4, Anti-p-Nrf2, Anti-HO-1, Anti-VDR and Anti-β-actin were purchased from Wuhan Saiweier Biotechnology Co., Ltd.

[0032] Cell culture. SH-SY5Y was purchased from the Cell Bank of the Chinese Academy of Sciences (Shanghai, China). Cells were cultured in DMEM containing 10% FBS in an incubator at 37°C with 5% CO2.

[0033] MPP + In vitro cell viability induced by MPP. Cell viability was measured using CCK-8 assay. SH-SY5Y cells were treated with MPP + SH-SY5Y cells were treated with MPP (3 mM) and different concentrations of AST (5, 10, 20, 40, 80, 100 μM) for 24 hours. +(3mM) and different concentrations of cycloastragenol (5, 10, 20, 40, 80, 100μM) were treated for 24 hours. Then, CCK-8 solution was added to each well, incubated at 37°C for 1 hour, and the absorbance was measured at 450nm using a microplate reader. According to the detection requirements of the LDH detection kit, the cell supernatant of each group was collected and added to the detection reagent. The absorbance value was measured at 450nm, and the LDH content in each group was calculated.

[0034] Animals. All C57BL / 6 mice were purchased from Beijing Weitonglihua Experimental Animal Co., Ltd., and all animal procedures were approved by the Animal Experiment Ethics Committee of Shanxi University of Traditional Chinese Medicine (AWE202307367). A total of 60 C57BL / 6 mice (male, 6-8 weeks, body weight 20±2g) were used in this study and divided into 4 groups (n=15): control group, MPTP group, AST-L group (10mg / kg) and AST-H group (30mg / kg). The mouse PD model was established by intraperitoneal injection of MPTP once a day for one week, with a concentration of 15mg / kg on the first day; 20mg / kg on the second day; and 30mg / kg on days 3 to 7. Starting from the first day of preparation of the MPTP group, AST treatment was once a day for 14 days.

[0035] Behavioral experiment. Gait measurement. The DigiGait animal gait detection system was used to evaluate the gait behavior indicators of mice. The speed was set to 15 cm / s, and the stride length and frequency of the paws of different groups of mice were recorded for 10 seconds.

[0036] Pole climbing test. Place the mouse on an experimental rod (1 cm in diameter, 60 cm in length) and record the time the mouse stays on the rod and the time it takes to descend to the bottom. The test is repeated three times with a 5-minute interval between each test.

[0037] Brain tissue transcriptomic analysis. Brain tissues (n=6) were collected from the control group, model group, and AST-H group, and total RNA was extracted from each sample. Sequencing was completed by the company. The main steps included RNA library construction, sequencing, differentially expressed genes, functional analysis (gene ontology analysis and pathway enrichment analysis), and the differentially expressed genes and functional analysis were divided into the control group and the model group, and the model group and the AST-H group. Then, the common differentially expressed genes between the model group and the AST-H group were screened for analysis.

[0038] Brain tissue metabolomics analysis Brain tissues (n=6) were collected from the control group, model group, and AST-H group, and the company was commissioned to perform sample processing and LC-MS analysis, including differential metabolite analysis and identification, differential substance analysis (differential substance cluster analysis and KEGG analysis, etc.), univariate statistical analysis, and multivariate statistical analysis. Finally, the differential substances between the control group and the model group, and between the model group and the AST-H group were obtained, and the metabolic pathways were analyzed.

[0039] Fluorescence quantitative PCR. Brain tissues of the control group, model group, and AST-H group were collected, and total RNA was extracted using a spin column animal total RNA purification kit and reversely transcribed into cDNA. SGExcel fast SYBR mixture was mainly used for the reaction on the fluorescence quantitative PCR instrument. GAPDH was used as an internal reference gene, and 2 -ΔΔCT Methods Relative gene expression levels were analyzed. The above experiment was repeated three times for calculation and analysis. Based on RNA-seq data analysis, PD-related differentially expressed genes were identified, and primers were designed and synthesized by a limited company. The primer sequences are shown in Table 1 below.

[0040] Table 1. Primer sequences of differentially expressed genes

[0041]

[0042] Analysis of inflammatory factors. Brain tissues and serum were collected from the control group, model group, and AST group, and the supernatant was extracted. ELISA analysis of inflammatory factors (IL-1β, IL-6, and TNF-α) was performed, and the absorbance value was measured at 450 nm to analyze the expression level of inflammatory factors.

[0043] Immunofluorescence analysis. Three mice were taken from each group for immunofluorescence staining. Mice were anesthetized with isoflurane, and 10 mL of PBS solution and 30 mL of 4% paraformaldehyde were perfused through the abdominal aorta. The tissue was washed three times with PBS. After dehydration with different concentrations of sucrose gradient, it was embedded in OCT reagent. The brain tissue was frozen in liquid nitrogen, and coronal sections (10 μm) were cut using a cryostat microtome. The slices were dried for 24 hours and stored at -80°C. The slices were washed with PBS and the OCT embedding agent was removed. The slices were immersed in PBS containing 0.3% Triton X-100 and incubated at room temperature for 30 minutes. The primary antibodies (TH and Iba-1) were evenly added to the slices and incubated overnight. Then, incubated with secondary fluorescent antibodies. Finally, DAPI was added and incubated for 5-10 minutes. Images were observed and captured using a laser confocal microscope, and fluorescence intensity or cell counts were analyzed using Image-J software.

[0044] Prussian blue staining. After brain tissue sectioning, remove paraffin and immerse in Prussian blue staining solution for 20-30 minutes. Rinse with distilled water and stain in nuclear fixative red staining solution for 5-10 minutes. After sealing the sections with glue, observe under an inverted fluorescence microscope and take photos at 200μm and 100μm magnification.

[0045] Protein expression analysis. Brain tissue and cell samples from different groups were collected and added to RIPA lysis buffer to extract total protein. Proteins were separated by SDS-PAGE (8%, 12% gel) and then transmembrane. 5% skim milk was used to block the polyvinylidene fluoride membrane. Subsequently, the membrane was incubated with Anti-TH, Anti-Iba-1, Anti-TfRC, Anti-FTH, Anti-Fpn, Anti-p-Nrf2, Anti-HO-1, Anti-GPX4, Anti-VDR and Anti-β-actin (1:1000) at 4°C overnight. TBST was used to wash the membrane. The membrane was incubated with anti-rabbit / anti-mouse secondary antibody (1:5000). Finally, the gel imaging system captured the development signal.

[0046] Statistical analysis. Statistical comparisons among groups were performed using one-way ANOVA followed by Tukey post-test. Data are presented as mean ± SD of three independent replicates. P values ​​< 0.05 were considered statistically significant.

[0047] result 1

[0049] AST can improve the in vitro and in vivo pharmacological indicators of PD models. First, we detected the cell viability and LDH expression level of AST in the in vitro PD model. The results showed that with the increase of AST concentration, cell viability reached a peak at 40-80μM, and the expression level of LDH decreased with the increase of cell viability, indicating that AST can reverse MPP + induced neuronal damage and has a neuroprotective effect. Figure 1 BC)

[0050] We constructed an MPTP-induced PD model in vivo and tested the pharmacological and pathological indicators of AST in improving PD. The results of behavioral experiments showed that MPTP induction could increase the gait frequency and shorten the stride length of mice in the gait experiment, which is consistent with the behavioral state of the PD model. After AST treatment, both stride length and gait frequency were significantly improved and tended to the control group. ( Figure 1 EF) In the pole climbing test, the time that the mice in the model group stayed at the top increased significantly, indicating that the mice had cognitive and behavioral disorders. After AST treatment, the climbing speed of the mice increased significantly. Figure 1G) Abnormal aggregation of α-synuclein is a typical pathological symptom of PD. Further pathological examination of PD showed that after administration, AST promoted the elimination of α-synuclein. ( Figure 1 H) 2

[0052] AST can alleviate MPTP-induced neuroinflammation. Since astragaloside IV is a precursor compound of AST, it has a significant inhibitory effect on neuroinflammation. Therefore, we studied the therapeutic effect of AST on MPTP-induced neuroinflammation. First, ELISA analysis was used to detect the expression of inflammatory factors in serum and brain tissue. The results showed that AST reversed the increase in the expression of inflammatory factors caused by MPTP in serum and brain tissue, and was positively correlated with the administered dose. ( Figure 2 AB) In addition, the activation level of microglia in the substantia nigra pars compacta (SNpc) was analyzed by immunofluorescence staining and western blotting. The results showed that in the SNpc, the number of TH-positive cells in the model group was significantly reduced, and AST could restore the reduction of TH expression; ( Figure 2 CE) At the same time, the model group caused an increase in the expression level of Iba-1, indicating that MPTP can stimulate the activation of microglia. After AST treatment, the expression of Iba-1 was downregulated, indicating that AST can inhibit the inflammatory response induced by MPTP. Figure 2 FI) 3

[0054] AST may affect neuroinflammation by regulating amino acid metabolic pathways. To further explore the pharmacological mechanism of AST in neuroinflammation, we used metabolomics to analyze the differential metabolites in brain tissues of different groups and analyzed the metabolic pathways based on the differential metabolites. The results showed that the regions of different groups were significantly different in multivariate statistical analysis and pairwise intergroup analysis under PLS-DA analysis, indicating that the differences between groups were good. ( Figure 3 A) In the differential metabolite analysis, the model group resulted in 4 up-regulated metabolites and 4 down-regulated metabolites compared with the control group. After AST treatment, CAG resulted in 7 up-regulated metabolites and 17 down-regulated metabolites compared with the model group. (Table 2 and Figure 3 C) In the KEGG analysis based on differential metabolites, arginine and proline metabolism, amino acid and cofactor biosynthesis emerged as the main metabolic pathways regulated by AST after drug administration. Figure 3B) Studies have shown that amino acid metabolic pathways dominated by arginine and proline metabolism are particularly important in neurological diseases, especially in regulating neuroinflammation levels. The biosynthesis of cofactors is related to the nutrition of neurons, and MPTP, as a neurotoxic substance, can significantly reduce the expression of neurotrophic factors such as BDNF. After AST treatment, it can nourish neurons and improve the function of nerve cells by restoring cofactors or neurotrophic substances. Therefore, the role of AST in improving neuroinflammation may be achieved through pathways such as amino acid metabolism and cofactor biosynthesis.

[0055] Table 2. Differential metabolites between Model and AST-H groups

[0056] 4

[0058] AST increased the expression of VDR gene, indicating that it regulates the ferritin deposition signaling pathway. Transcriptomics was used to explain the neuroinflammatory pharmacological effects of AST at the mRNA level. According to the screening criteria (fold change >2 or <0.5, p<0.05), the differentially expressed gene results of Control+Model and Model+AST-H were obtained. In the Control and Model groups, a total of 48 and 32 genes were upregulated and downregulated. In Model+CAG-H, a total of 39 and 8 genes were upregulated and downregulated. ( Figure 4 C) By summarizing the differentially expressed genes, we screened genes related to PD or neuroinflammation for GO and KEGG analysis, with p < 0.05 as the screening criterion. Finally, we identified 7 differentially expressed genes related to the model group (Cd74, Mst1, Ccr2, Cnn1, Retnlg, VDR, and Cd200r1) and verified them using fluorescent quantitative PCR technology. The results showed that the mRNA expression of VDR, Cnn1, and Retnlg was consistent with the transcriptome analysis. ( Figure 4 DF) In the gene function analysis, VDR is a vitamin D receptor that plays an important role in the nervous system by binding to various ligands, especially in the study of neurodegenerative diseases, where it can mediate various physiological functions such as oxidative stress and ferroptosis. Cnn1 is a calmodulin protein, and recent studies have found that its binding to the Kdm6a enzyme can affect neuroinflammation and neural function repair. The Retnlg gene is associated with various physiological processes such as metabolic disorders, immune function, and inflammation. In the GO analysis, the results of Model vs AST-H include "response to external stimuli", "cellular response to chemical stimuli", and "signal receptor binding". ( Figure 4 B) For KEGG analysis, the model group and AST-H group were enriched in "neurogenesis pathways in multiple diseases" and other related diseases, as well as common inflammatory pathways such as IL-17, MAPK, and HIF-1 signaling pathways. ( Figure 4 A) In addition, we noticed that ferroptosis may exist in the pathological process in which AST exerts its pharmacological effects. Therefore, we conducted experimental verification around the VDR gene and the ferroptosis signaling pathway. In the protein expression detection, the Western Blot results were consistent with the PCR results. The expression of VDR receptor in the model group was reduced, while the VDR expression level was significantly upregulated after AST treatment. ( Figure 4 GH) 5

[0060] AST plays an anti-neuroinflammatory role by reducing oxidative stress levels and inhibiting ferroptosis pathways. We first used Prussian blue staining to analyze the accumulation of iron ions in the brains of mice in different groups. The results showed that after MPTP induction, iron accumulation in the model group was significantly aggravated, blue plaques increased, and AST could effectively reduce brain iron levels. Figure 5 A) In addition, the expression levels of ferritin-related proteins were detected by Western blotting. The results showed that compared with the model group, the expression of TfRC (iron transporter) and FTH (iron storage protein) was significantly reduced after AST treatment, while the expression of Fpn (iron efflux protein) was upregulated, indicating that AST can reverse MPTP-induced cellular iron storage, inhibit intracellular iron transport, and accelerate iron ion efflux. Glutathione peroxidase 4 (GPX4) is a key factor in the process of ferroptosis and can be used as one of the indicators for determining cellular ferroptosis. Therefore, in the protein expression results, it was found that in the MPTP-induced model, the expression level of GPX4 was significantly reduced, resulting in intracellular peroxide accumulation, while AST treatment can significantly upregulate the expression level of GPX4. ( Figure 5 BF)

[0061] In order to explore the effect of MPTP-induced oxidative stress, the Nrf2 / HO-1 signaling pathway is a key pathway of the antioxidant system in the body. Nrf2 can repair the function of the glutathione system, and at the same time, Nrf2 can regulate the expression of iron metabolism-related proteins in ferroptosis and improve ferroptosis. Therefore, we detected the phosphorylation level of Nrf2 and the expression of HO-1. The results showed that the phosphorylation level of Nrf2 in the model group was significantly reduced, and the expression of HO-1 protein was reduced. After AST treatment, the expression of p-Nrf2 and HO-1 increased significantly, indicating that AST can activate the Nrf2 / HO-1 signaling pathway in vivo and exert an antioxidant effect. ( Figure 5 GI) 6

[0063] The in vitro cytotoxicity of cycloastragenol at high doses has been reported in the literature and is also a potential drawback of cycloastragenol. The activity comparison between cycloastragenol and astragenol (AST) was evaluated by using an in vitro Parkinson's cell model (MPP+ induced SH-SY5Y cells). It was found that at a concentration of 20-40μM, the activity of astragenol (AST) was slightly worse than that of cycloastragenol, but it is worth noting that in the LDH (lactate dehydrogenase assay, the purpose of evaluating potential cell toxicity) assay, at a concentration of 100μM, the in vitro cytotoxicity of astragenol (AST) was significantly lower than that of cycloastragenol. This exploration can further prove that the breakage of the bridge ring in the structure is beneficial to the change in the activity of the compound.

[0064] in conclusion

[0065] In summary, this study explored the potential application of AST in neurodegenerative diseases and found that AST can inhibit the progression of neuroinflammation and alleviate the symptoms of PD. In addition, through multi-omics analysis and verification experiments, ferroptosis is a key pathway for AST to inhibit neuroinflammation. AST can reduce the level of oxidative stress in cells, thereby regulating neuronal homeostasis and protecting neurons. This finding demonstrates the potential application of AST in neuroprotection, provides a scientific basis for the development of drugs or dietary supplements, and lays a data support for the comprehensive elucidation of the development and application of Astragalus in "medicine and food homology".

[0066] The present invention has been described in detail above. It will be apparent to those skilled in the art that the present invention may be implemented in a wide range under equivalent parameters, concentrations and conditions without departing from the spirit and scope of the present invention and without the need for unnecessary experimentation. Although the present invention provides specific embodiments, it should be understood that further improvements may be made to the present invention. In short, according to the principles of the present invention, this application intends to include any changes, uses or improvements to the present invention, including changes made by conventional techniques known in the art that depart from the scope disclosed in this application. Applications of some of the basic features may be made within the scope of the following appended claims.

Claims

1. Application of astragalool in the preparation of products for treating or alleviating Parkinson's disease.

2. The use according to claim 1, characterized in that: The product is a medicine or a health product.

3. The use according to claim 2, characterized in that: The health product is a dietary supplement.

4. The use according to claim 2, characterized in that: The treatment or alleviation of Parkinson's disease is embodied in: 1) Relieve movement disorders caused by MPTP; 2) Reduce inflammatory factors in serum and brain tissue; 3) Improve the abnormal aggregation of α-synuclein.

5. A product for treating or alleviating Parkinson's disease, characterized in that: The active ingredient of the product includes astragalool.

6. The product according to claim 5, characterized in that The product is a medicine or a health product.

7. The product according to claim 6, characterized in that The health product is a dietary supplement.

8. The product according to claim 6, characterized in that The treatment or alleviation of Parkinson's disease is embodied in: 1) Relieve movement disorders caused by MPTP; 2) Reduce inflammatory factors in serum and brain tissue; 3) Improve the abnormal aggregation of α-synuclein.

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