Use of Lycium barbarum glycopeptide in the preparation of drugs for treating drug-induced motor complications of Parkinson's disease

Abstract

The present invention belongs to the field of biomedicine, and in particular to the use of Lycium barbarum glycopeptide in the preparation of a medicament for preventing or treating drug-induced Parkinson's disease (PD) motor complications. Preferably, Lycium barbarum glycopeptide is used as a partner drug of levodopa to prevent or treat levodopa-induced dyskinesia. The present invention uses levodopa-induced dyskinesia (LID) animal models of 6-hydroxydopamine midbrain substantia nigra localized injection and levodopa intraperitoneal injection modeling as research objects, and studies the effect of Lycium barbarum glycopeptide in improving LID. The results showed that Lycium barbarum glycopeptide can significantly improve drug-induced PD motor complications LID, indicating that Lycium barbarum glycopeptide can be used as a partner drug to assist levodopa in treating PD.

Description

Technical Field

[0001] The present invention belongs to the field of biomedicine, and specifically relates to the use of Lycium barbarum glycopeptide in preparing a drug for preventing or treating drug-induced motor complications of Parkinson's disease. Background Art

[0002] Parkinson's disease (PD), also known as Parkinson's paralysis, is a chronic neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta of the midbrain and the appearance of Lewy bodies within neurons. Epidemiological data show that the prevalence rate among people over 60 years old is 2%, a significant burden that urgently needs to be addressed in our aging society. For half a century, dopamine replacement therapy, primarily based on levodopa, has been the gold standard for PD treatment. Levodopa can cross the blood-brain barrier and deacidify to form dopamine. While supplementation of this neurotransmitter can temporarily alleviate behavioral abnormalities, it cannot prevent neuronal degeneration. Because patients are forced to take medication throughout their lives to improve their symptoms, as the disease progresses and the therapeutic dose increases, most patients develop numerous motor complications, such as levodopa-induced dyskinesias, which severely impact their quality of life and are a major cause of disability in Parkinson's patients.

[0003] Levodopa-induced motor complications primarily include motor fluctuations and dyskinesia (LID). Based on clinical manifestations, the former can be divided into four types: wearing-off phenomenon, delayed on-time, on-off phenomenon, and freezing of gait, while the latter can be divided into three types: peak-dose dyskinesia, off-time dystonia, and biphasic dyskinesia. Levodopa use is an independent risk factor for motor complications. Due to its short half-life and rapid absorption and metabolism, fluctuations in blood concentrations can affect signaling pathways such as D1 / 2 receptors, glutamate receptors, and serotonin receptors, leading to a complex cascade of reactions involving both neurons and non-neurons. The pathological mechanisms are difficult to elucidate, the most classic of which is disruption of the dopamine system. Levodopa can repeatedly stimulate the dopamine D1 receptor, leading to increased protein kinase activity and a series of cascade reactions. First, adenylate cyclase is activated by the D1 receptor, promoting the phosphorylation of dopamine and cAMP-regulated phosphoprotein-32 (DARPP-32), which in turn promotes the phosphorylation of extracellular regulated protein kinase (ERK) and increased expression of the early gene protein Delta FosB, ultimately leading to the "defunctionalization" loss of synaptic signals and an imbalance in basal ganglia activity, thereby promoting the occurrence of dyskinesia.

[0004] In terms of treatment, aside from surgical procedures like deep brain stimulation and unilateral pallidum lesioning, currently available medications are very limited, primarily including amantadine, monoamine oxidase B inhibitors, and catechol-O-methyltransferase inhibitors. These treatments often lack sustained efficacy and can introduce new side effects. Currently, there is still a lack of effective treatments for drug-induced motor complications, placing patients in a long-term dilemma regarding the use of anti-PD medications. The development of treatment strategies remains a significant challenge.

[0005] In Traditional Chinese Medicine (TCM), Parkinson's disease (PD) falls under the category of "tremor syndrome," with descriptions of its symptoms dating back to the Yellow Emperor's Classic of Internal Medicine. Ming Dynasty physician Sun Yikui first named PD "tremor syndrome" in his book "Chishui Xuanzhu," and scholars throughout history have subsequently developed corresponding discussions and accumulated experience. Based on the pathogenesis of this disease, which is characterized by deficiency in the underlying cause and excess in the superficial symptoms, TCM-guided treatment for motor complications primarily targets the underlying mechanisms of "wind, fire, phlegm, blood stasis, and deficiency," emphasizing calming the liver and extinguishing wind, and nourishing the liver and kidneys. This approach prioritizes the treatment of "tremor syndrome," emphasizing liver-soothing, suppressing yang, and extinguishing wind. Simultaneously, detoxifying and expelling pathogenic factors are administered to regulate the patient's internal organs and balance qi, blood, yin, and yang, aiming to address both the underlying cause and the underlying symptoms.

[0006] Goji berries, a traditional Chinese medicine, are the mature fruit of the Ningxia wolfberry, a plant of the Solanaceae family. They have been hailed as a precious Chinese herbal medicine since ancient times and are used in a variety of tonic prescriptions. The "Shennong Bencao Jing" states: "Goji berries treat internal pathogens, heat-induced thirst, rheumatism, and rheumatism. Long-term consumption strengthens the bones and muscles, promotes lightness and anti-aging, and provides resistance to cold and heat." Its sweet and mild flavor nourishes the kidneys, moistens the lungs, tonifies the liver, dispels wind, and improves eyesight. It treats liver and kidney yin deficiency, soreness of the waist and knees, dizziness, and vertigo. Its medicinal and edible properties are a strength of goji berries, offering promising development prospects. Modern pharmacological research has shown that goji berries possess neuroprotective, free radical scavenging, and anti-inflammatory properties, making them widely used in health and wellness.

[0007] Lycium barbarum glycopeptide (LbGP) is an immunologically active component first discovered in wolfberry by Tian Gengyuan's team at the Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences. It is a glycoconjugate consisting of a covalently bound polysaccharide and a peptide chain. It consists of five components (LbGp1, LbGp2, LbGp3, LbGp4, and LbGp5), with a well-defined three-dimensional structure and identification methods. Its preparation methods include pure physical centrifugation, membrane filtration purification, and vacuum freeze-drying. Lycium barbarum glycopeptide differs from previously studied wolfberry polysaccharides. LbGP is a general term for a class of crude polysaccharides found in wolfberries, composed of six monosaccharides: glucose, galactose, mannose, and arabinose. The content of LbGP in wolfberries is approximately 2%-5%. The Chinese Pharmacopoeia requires that the LbGP content in wolfberries must be no less than 1.8% (calculated as glucose).

[0008] Previous studies have shown that Lycium barbarum polysaccharides can play a certain protective role in PD. The inventors' team also found in their previous research on Lycium barbarum glycopeptides that they can improve PD (see CN113750217A), but there have been no reports on Lycium barbarum glycopeptides as a levodopa partner drug to alleviate drug-induced motor complications of PD. Summary of the Invention

[0009] To address the problem of a lack of existing drugs that can effectively prevent or treat drug-induced motor complications of Parkinson's disease, the present invention provides the use of Lycium barbarum glycopeptide in the preparation of a drug for preventing or treating drug-induced motor complications of Parkinson's disease. In particular, the present invention provides the use of Lycium barbarum glycopeptide as a levodopa chaperone in the preparation of a drug for treating drug-induced motor complications of Parkinson's disease.

[0010] Specifically, the present invention is achieved through the following technical solutions:

[0011] The present invention provides use of Lycium barbarum glycopeptide in preparing a medicament for preventing or treating drug-induced motor complications of Parkinson's disease.

[0012] As an alternative, in the above use, the motor complications of Parkinson's disease are levodopa-induced.

[0013] As an option, in the above use, the Parkinson's disease motor complications include movement fluctuations and dyskinesias.

[0014] As an optional method, in the above-mentioned use, the movement complications include abnormal involuntary movements of the axial, limb and orofacial regions, wherein the abnormal involuntary axial movements are twisting movements of the neck and upper body toward the contralateral side of the injury, the abnormal involuntary limb movements are repetitive jumping or dystonia postures of the contralateral forelimbs, and the abnormal involuntary movements of the orofacial region are jaw movements and contralateral tongue protrusion.

[0015] As an optional mode, in the above use, Lycium barbarum glycopeptide is used as a partner drug of levodopa to prevent or treat levodopa-induced dyskinesia (LID).

[0016] This study uses behavioral data from LID as the optimal indicator for LID improvement. By detecting and calculating the score of abnormal involuntary movements (AIMs), it was demonstrated that Lycium barbarum glycopeptide can significantly improve LID. In this study, the improvement in AIMs includes scores for the axial, limb, and orofacial components. Observation was conducted every 30 minutes after levodopa administration, for a total of 120 minutes.

[0017] The present invention uses the expression of tyrosine hydroxylase TH (a marker of dopaminergic neurons), the expression of DeltaFosB and the phosphorylation of ERK1 / 2 (closely related to the occurrence of LID) in the mouse midbrain as pathological indicators for LID improvement. The above indicators were analyzed by protein immunoblotting to prove that wolfberry glycopeptide can significantly improve LID.

[0018] The pathogenic mechanisms of LID are diverse. In the present invention, 6-hydroxydopamine (6-OHDA) is used to simulate neurotoxicity to cause nerve cell damage leading to PD, and L-dopa is used to induce LID symptoms in an animal model.

[0019] As an optional mode, in the above use, the dosage of the Lycium barbarum glycopeptide for preventing or treating drug-induced motor complications of Parkinson's disease is 1-100 mg / kg.

[0020] Preferably, the dosage of the Lycium barbarum glycopeptide for preventing or treating drug-induced motor complications of Parkinson's disease is 30 mg / kg.

[0021] As an optional method, in the above-mentioned use, the preparation method of the wolfberry glycopeptide mainly includes the steps of washing, soaking, crushing and beating, extraction, double-pass beating, two-stage separation, membrane separation, single-effect concentration, and freeze-drying. In particular, the wolfberry seeds are separated in the double-pass beating step, the wolfberry pulp is separated in the two-stage centrifugation step, and the oligosaccharides are separated in the membrane separation step, and the final product obtained is the wolfberry glycopeptide.

[0022] As an optional mode, in the above use, the Lycium barbarum glycopeptide comprises one or more of the following: LbGp1, LbGp2, LbGp3, LbGp4 or LbGp5.

[0023] Among them: the protein content in LbGp1 is 28.87%, the protein content in LbGp2 is 9.25%, the protein content in LbGp3 is 5.19%, the protein content in LbGp4 is 10.75% and the protein content in LbGp5 is 59.87%.

[0024] As an optional manner, in the above-mentioned use, the Lycium barbarum glycopeptide contains LbGp1, LbGp2, LbGp3, LbGp4 and LbGp5, wherein the mass ratio of LbGp1, LbGp2, LbGp3, LbGp4 and LbGp5 is (0.01-0.02): (0.005-0.01): (0.01-0.02): (0.02-0.03): (0.01-0.02).

[0025] Preferably, in the Lycium barbarum glycopeptide, the mass ratio of LbGp1, LbGp2, LbGp3, LbGp4 and LbGp5 is 0.018:0.0077:0.018:0.029:0.014.

[0026] As an optional mode, in the above use, the medicine comprises Lycium barbarum glycopeptide and a pharmaceutically acceptable carrier.

[0027] As an optional mode, in the above use, the dosage form of the drug is tablets, pills, oral liquid, capsules, syrups, pellets, granules, injections, powder injections, sprays, aerosols, powder sprays or suppositories.

[0028] Compared with the prior art, the present invention has the following beneficial effects:

[0029] This present invention proposes for the first time that Lycium barbarum glycopeptide can be used as a levodopa partner drug to prevent or treat levodopa-induced dyskinesia. Using LID animal models induced by targeted midbrain injection of 6-hydroxydopamine in the substantia nigra and intraperitoneal injection of levodopa, the present study investigated the effect of Lycium barbarum glycopeptide on LID. The results showed that Lycium barbarum glycopeptide significantly improved drug-induced LID, a motor complication of Parkinson's disease (PD), demonstrating its potential as a partner drug to complement levodopa in the treatment of PD. BRIEF DESCRIPTION OF THE DRAWINGS

[0030] The accompanying drawings are used to provide a further understanding of the present invention and constitute a part of the specification. Together with the embodiments of the present invention, they are used to explain the present invention and do not constitute a limitation of the present invention. In the accompanying drawings:

[0031] Figure 1 The construction and validation of the PD model are shown;

[0032] Figure 2 Shows the LID modeling and grouping and drug administration process;

[0033] Figure 3 The results showed that the modeling and drug administration methods had no significant effect on the body weight of mice;

[0034] Figure 4 Shown are the effects of each group of drugs on the axial scores of abnormal involuntary movements of mice;

[0035] Figure 5 Shown are the effects of each group of drugs on the limb direction scores of abnormal involuntary movements of mice;

[0036] Figure 6 Shown are the effects of each group of drugs on the oral-facial scores of abnormal involuntary movements in mice;

[0037] Figure 7 Shown are the effects of each group of drugs on the total score of abnormal involuntary movements of mice;

[0038] Figure 8 Shown are the effects of each group of drugs on the expression of TH protein in the striatum of mice;

[0039] Figure 9 Shown are the effects of each group of drugs on the expression of Delta FosB protein in the striatum of mice;

[0040] Figure 10 Shown are the effects of each group of drugs on the phosphorylation and activation of ERK1 / 2 in the mouse striatum. DETAILED DESCRIPTION

[0041] The present invention provides the use of Lycium barbarum glycopeptide to improve PD motor complications. Those skilled in the art can refer to the content of this article and appropriately improve the process parameters to achieve the purpose. It should be noted in particular that all similar replacements and modifications are obvious to those skilled in the art and are considered to be included in the present invention. The methods and applications of the present invention have been described through preferred embodiments, and relevant personnel can obviously modify or appropriately change and combine the methods and applications herein without departing from the content, spirit and scope of the present invention to implement and apply the technology of the present invention.

[0042] If no specific techniques or conditions are specified in the examples, the experiments were carried out according to the techniques or conditions described in the literature in the field or according to the product instructions. If no manufacturer is specified for the reagents or instruments used, they are all conventional products that can be purchased through regular channels.

[0043] The experimental methods in the following examples are conventional methods unless otherwise specified. The experimental materials used in the following examples are commercially available products unless otherwise specified.

[0044] The preparation of the Lycium barbarum glycopeptide of the present invention involves extracting and isolating an aqueous extract of Lycium barbarum through pure physical centrifugation, membrane filtration purification, and vacuum freeze-drying to obtain a glycoconjugate of a polysaccharide covalently bound to a peptide chain. The glycoconjugate comprises LbGp1, LbGp2, LbGp3, LbGp4, and LbGp5. The protein content of LbGp1 is 28.87%, that of LbGp2 is 9.25%, that of LbGp3 is 5.19%, that of LbGp4 is 10.75%, and that of LbGp5 is 59.87%. The mass ratio of LbGp1, LbGp2, LbGp3, LbGp4, and LbGp5 in the Lycium barbarum glycopeptide is 0.018:0.0077:0.018:0.029:0.014.

[0045] The present invention will be further described below in conjunction with the embodiments:

[0046] Example 1

[0047] 1. Experimental Materials and Instruments

[0048] 1. Experimental Animals

[0049] C57BL / 6J male mice, 6 weeks old, weighing 20 - 22 g, were purchased from the Laboratory Animal Management Center of Southern Medical University (License: SCXK(Yue)2021 - 0041). The animals were housed in the Medical Experimental Animal Center of Jinan University at a temperature of 23 ± 2°C and a humidity of 50 ± 10%, with standard mouse feed. The experimental animals in each group had free access to food and water.

[0050] 2. Main experimental reagents

[0051] Lycium barbarum glycopeptide (Ningxia Tianren Lycium barbarum Biotechnology Co., Ltd.), 6 - OHDA (Sigma, H4381), L - DOPA (Sigma, D9628), apomorphine (Sigma, A4393), BCA assay kit, TH antibody (Abcam, ab112), p - ERK antibody (Proteintech, 28733 - 1 - AP), ERK antibody (Proteintech, 11257 - 1 - AP), Delta FosB antibody (Cell Signaling Technology, 14695S), GAPDH antibody (Hangzhou Fude Biotechnology Co., Ltd., FD0063), β - Actin antibody (Hangzhou Fude Biotechnology Co., Ltd., FD0060), HRP - labeled goat anti - rabbit secondary antibody (Hangzhou Fude Biotechnology Co., Ltd., FDR007), HRP - labeled goat anti - rabbit secondary antibody (Hangzhou Fude Biotechnology Co., Ltd., FDR007).

[0052] 3. Main experimental instruments

[0053] Mouse stereotaxic apparatus (Shenzhen Reword Biotechnology Co., Ltd.), mouse rotarod (Ugo Basile, Italy), high - speed low - temperature centrifuge (Sartorius, Germany, A - 14C), chemiluminescent imaging system (Tanon - 5200), electronic balance (Sartorius, Germany, BS210).

[0054] II. Experimental methods and results

[0055] 1. Preparation of LID model

[0056] First, a PD model was established using 6-OHDA. After seven days of adaptive feeding, mice were weighed and deeply anesthetized with 1% sodium pentobarbital. The head hair was shaved with a razor and the mice were fixed in a stereotaxic apparatus, with the left and right ear bars adjusted for more secure fixation. The skin of the mouse head was incised along the midline to expose the skull. The bregma and lambda were then wiped with hydrogen peroxide to fully expose the bregma. Using the bregma coordinate origin and referring to the Mouse Brain Stereotaxic Atlas, the injection coordinates were set at AP: +0.3, L: +2.3, and DV: -2.9. A small hole was carefully drilled with a skull drill (to avoid damaging brain tissue). 1.5 μL of 5 μg / μL 6-OHDA was slowly injected at a rate of 0.1 μL / min. The needle was left in place for 5 minutes, then slowly withdrawn. The scalp was sutured to complete the brain injection. 21 days after injection, APO (0.5 mg / kg) was injected intraperitoneally to induce mice to rotate toward the healthy side. The test was performed three times, each time for 10 minutes, and the average value was taken. The mice with more than 70 rotations were selected as successful models, and the other mice were eliminated. Figure 1 ).

[0057] Next, a LID model was established using levodopa. The PD model was intraperitoneally injected with levodopa (7.5 mg / kg) daily, and the successful establishment of the PD model was confirmed by 6-OHDA, with Day 0 being the day for a total of 42 days.

[0058] 2. Experimental Grouping and Weight Monitoring

[0059] The experimental mice were divided into 5 groups: 8 untreated mice were set as blank group (Sham). The mice with successful PD model were randomly divided into 4 groups, 8 in each group, namely: 6-OHDA group, 6-OHDA+levodopa group, 6-OHDA+levodopa+LbGp low-dose (30 mg / kg, gavage) group and 6-OHDA+levodopa+LbGp high-dose (60 mg / kg, gavage) group. The experimental process is as follows Figure 2 shown.

[0060] Weight monitoring: Figure 3 As shown, the body weight data for 6 consecutive weeks showed that the modeling and drug administration methods used in this experiment had no significant effect on the body weight of mice.

[0061] 3. Behavioral Methods and Results: Abnormal Involuntary Movement Scale (AIM)

[0062] Methods: The AIM score is divided into three parts, including axial, limb, and orofacial. Observations were conducted every 30 minutes after levodopa administration, with each observation lasting 1 minute for a total of 120 minutes. (1) Axial AIM: twisting movements of the neck and upper body toward the contralateral side of the injury; (2) Limb AIM: repetitive jumping or dystonic postures of the contralateral forelimb; (3) Orofacial AIM: open jaw movements and contralateral tongue protrusion. Each subtype was scored from 1 to 4 according to the intensity of the movement disorder during the observation period: 0: no movement disorder; 1: occasional occurrence (less than 30 seconds); 2: frequent occurrence (more than 30 seconds); 3: symptoms persisted and stopped after external stimulation; 4: symptoms persisted and did not stop after stimulation. The total AIM score was the cumulative score of each part during each observation period.

[0063] Experimental results: According to the abnormal involuntary movement score (AIM) principle, the effects of Lycium barbarum glycopeptide on LID induced by levodopa were evaluated. Figure 4-Figure 7 As shown, including the axial AIM score ( Figure 4 ), oral-facial AIM score ( Figure 5 ), limb-directed AIM score ( Figure 6 ) and AIM total score ( Figure 7 ). Compared with the 6-OHDA group alone, the AIM scores of mice in the levodopa group increased on the 7th, 21st and 42nd days. The longer the administration time, the higher the AIM score, indicating that long-term administration of levodopa induced LID behavioral disorders in the PD model. There was no significant difference in the improvement effect of low-dose Lycium barbarum glycopeptide (30 mg / kg) on ​​the AIM scores on the 7th day, but low-dose Lycium barbarum glycopeptide (30 mg / kg) could significantly alleviate the AIM scores of mice on the 21st and 42nd days. At the same time, high-dose Lycium barbarum glycopeptide (60 mg / kg) showed significant differences in the AIM scores on the 7th, 21st and 42nd days compared with the model group mice ( *** p<0.001vs.6-OHDA group, # p<0.05, ## p<0.005, ### p<0.001 vs. 6-OHDA+levodopa group, ns=not significant vs. 6-OHDA+levodopa group. N=8 mice in each group. The above data demonstrate that Lycium barbarum glycopeptide treatment can improve LID induced by levodopa.

[0064] 4. Pathological methods and results: Western blotting

[0065] Method Description: Rapidly remove bilateral striatum from mouse brains on ice. Approximately 10 mg of tissue was excised and placed in a 1.5 mL EP tube. Two steel beads were added to each sample. Protein lysis buffer premixed with protease inhibitors and phosphatase inhibitors was then added at a V / W ratio (10 μL:1 mg) (protease inhibitor: protein lysis buffer = 1:100, phosphatase inhibitor: protein lysis buffer = 1:50). The tissue was homogenized on a pre-chilled lead plate and sonicated to extract total protein. Protein concentration was determined using a BCA protein concentration assay kit. 30 μg of protein was separated by electrophoresis in a prepared SDS-polyacrylamide gel according to the molecular weight of the target protein, then electrotransferred to a PVDF membrane and blocked with 5% skim milk powder at room temperature for 2 h; primary antibodies (TH, p-ERK, ERK, GAPDH, β-Actin) were incubated overnight in a 4°C refrigerator; the primary antibodies were recovered and washed with TBST buffer, and each band was incubated with HRP-labeled goat anti-rabbit secondary antibody or goat anti-mouse secondary antibody at room temperature for 2 h; washed with TBST buffer, and photographed with ECL colorimetric solution on an imaging system; the results were analyzed using Image J software.

[0066] Experimental results: Tyrosine hydroxylase (TH) is the rate-limiting enzyme for dopamine synthesis in the midbrain and can be used as a marker for dopamine neurons. Compared with the normal group, the expression of TH in the striatum of mice in the 6-OHDA group was significantly decreased, indicating that the number of dopaminergic neurons was significantly reduced. L-dopa could not reduce the loss of TH, while Lycium barbarum glycopeptide could improve the loss of TH, proving that Lycium barbarum glycopeptide can protect dopaminergic neurons, such as Figure 8 As shown ( ** p<0.005, *** p<0.001, N=3 mice in each group). The occurrence of LID is closely related to Delta FosB. Compared with the 6-OHDA group, long-term administration of L-dopa significantly increased the expression of Delta FosB in the striatum of model mice, while Lycium barbarum glycopeptide could significantly improve the increase of Delta FosB, proving that Lycium barbarum glycopeptide can improve the degree of LID induced by L-dopa. Figure 9 As shown ( * p<0.005, N=3 mice in each group). In LID dyskinesia, phosphorylated extracellular regulated protein kinases (ERK1 / 2) are activated. Compared with the 6-OHDA group, long-term administration of L-dopa increased the expression of p-ERK1 / 2, that is, promoted the phosphorylation and activation of ERK1 / 2, while Lycium barbarum glycopeptide significantly inhibited the phosphorylation and activation of ERK1 / 2, proving that Lycium barbarum glycopeptide can improve the degree of LID induced by L-dopa. Figure 10 As shown (* p<0.005, ** p<0.005, N=3 mice in each group).

[0067] The above are only preferred embodiments of the present invention. It should be pointed out that for ordinary technicians in this technical field, several improvements and modifications can be made without departing from the principles of the present invention. These improvements and modifications should also be regarded as the scope of protection of the present invention.

Claims

1. Use of Lycium barbarum glycopeptide in the preparation of a medicament for treating levodopa-induced dyskinesia, characterized in that: Lycium barbarum glycopeptide is used as a partner drug of levodopa, and the Lycium barbarum glycopeptide contains LbGp1, LbGp2, LbGp3, LbGp4 and LbGp5, and the mass ratio of LbGp1, LbGp2, LbGp3, LbGp4 and LbGp5 is 0.018:0.0077:0.018:0.029:0.

014.

2. The use according to claim 1, characterized in that: The dosage of the Lycium barbarum glycopeptide for treating levodopa-induced dyskinesia is 30 mg / kg or 60 mg / kg.

3. The use according to claim 1, characterized in that: The medicine comprises wolfberry glycopeptide and a pharmaceutically acceptable carrier.

4. The use according to claim 1, characterized in that: The dosage form of the medicine is tablet, pill, oral liquid, capsule or granule.

5. The use according to claim 1, characterized in that: The dosage form of the medicine is drop pill or syrup.

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