Use of propargyl cysteine in the preparation of a drug for treating breast hyperplasia

Abstract

This invention relates to a novel use of propargylcysteine ​​in the preparation of anti-mastopathy drugs. The invention discovers that S-propargylcysteine ​​can improve E2 / P imbalance by regulating HPO axis function and inhibiting abnormal activation of the GnRH-sex hormone axis; it also reduces the inflammatory microenvironment by inhibiting the release of inflammatory factors; ultimately, it downregulates ER / PR-mediated proliferation signals and inhibits PCNA expression locally in the breast. Through multi-target regulation of neuroendocrine, inflammatory responses, and proliferation-related signaling pathways, it effectively alleviates breast hyperplasia and its associated chronic stress-induced depressive-like behaviors, thus exerting anti-mastopathy and therapeutic effects on breast hyperplasia complicated with depression.

Description

Technical Field

[0001] This invention belongs to the field of pharmaceutical technology and relates to a new pharmaceutical use of propargylcysteine, specifically the use of propargylcysteine ​​in the preparation of anti-mastopathy drugs. Background Technology

[0002] Breast hyperplasia with depression is a psychosomatic disease driven by endocrine imbalance and psychosocial factors. Its main characteristics include proliferative changes in breast tissue accompanied by mood disorders (such as persistent low mood, loss of interest, and anxiety). This disease is usually closely related to estrogen / progesterone imbalance and hypothalamic-pituitary-ovarian axis (HPO axis) dysfunction. Chronic psychological stress further exacerbates endocrine imbalance and pathological changes in breast tissue through neuroendocrine pathways (such as the hypothalamic-pituitary-adrenal axis and HPA axis). Core risk factors include long-term mental stress, mood swings, sleep disorders, endocrine disorders, menstrual irregularities, and unhealthy lifestyle habits. With the accelerated pace of modern life and increased psychological stress, the incidence of breast hyperplasia with depression is rising year by year, becoming a significant issue affecting women's physical and mental health, and potentially increasing the risk of breast disease progression and decreased quality of life. Current clinical treatment often involves a combination of endocrine-regulating drugs and antidepressants, but overall efficacy varies among individuals, and some patients experience adverse reactions and relapse risks. Therefore, exploring safe and effective treatment strategies that can both regulate endocrine function and improve mood is of great significance for the prevention and treatment of this type of disease. Summary of the Invention

[0003] Therefore, the purpose of this invention is to provide a new drug that can be used to treat breast hyperplasia complicated with depression.

[0004] The technical solution of the present invention includes the following.

[0005] This invention provides the use of S-propynylcysteine ​​or a pharmaceutically acceptable salt thereof in the preparation of medicaments for improving or treating breast hyperplasia.

[0006] The present invention also provides the use of S-propynylcysteine ​​or a pharmaceutically acceptable salt thereof in the preparation of medicaments for improving or treating breast hyperplasia complicated with depression.

[0007] This invention discovers that S-propynylcysteine ​​can improve E2 / P imbalance by regulating HPO axis function and inhibiting abnormal activation of GnRH-sex hormone axis; it also reduces the inflammatory microenvironment by inhibiting the release of inflammatory factors; and ultimately downregulates ER / PR-mediated proliferation signaling and inhibits PCNA expression in the breast. Through multi-target regulation of neuroendocrine, inflammatory response and proliferation-related signaling pathways, it effectively alleviates breast hyperplasia and its associated chronic stress-induced depressive-like behavior, thus playing a role in anti-breast hyperplasia and treatment of breast hyperplasia complicated with depression.

[0008] S-Propylcysteine ​​is a known drug with multiple biological functions, including anti-inflammatory, antioxidant, and metabolic disorder-improving effects, exhibiting good bioavailability, stability, and completeness. Its application in treating breast hyperplasia and breast hyperplasia complicated with depression provides a safer and more effective treatment option for breast hyperplasia and related diseases. Attached Figure Description

[0009] Figure 1 This study demonstrates the effect of the sucrose preference assay on depressive behavior in HMG rats. Data are presented as mean ± standard deviation (mean ± SD) (n=10). Statistical analysis was performed using one-way ANOVA. **P < 0.01, compared with the control group; #P < 0.05, ##P < 0.01, ###P < 0.001, compared with the model group.

[0010] Figure 2 This study demonstrates the effect of SPRC on nipple height and diameter in HMG rats. Data are expressed as mean ± standard deviation (mean ± SD) (n=10). Statistical analysis was performed using one-way ANOVA. ***P < 0.001, compared with the control group; #P < 0.05, ##P < 0.01, ###P < 0.001, compared with the model group; ns indicates no statistically significant difference (P > 0.05).

[0011] Figure 3 This image shows the pathological changes in mammary gland tissue of HMG rats after SPRC treatment.

[0012] Figure 4 SPRC showed that it significantly reduced the expression of hormone-related receptors ER, PR, and PCNA in mammary tissue of HMG rats.

[0013] Figure 5 SPRC showed that it significantly reduced the expression of GnRH in the hypothalamus of HMG rats.

[0014] Figure 6This study demonstrated that SPRC regulates p-AKT expression in mammary tissue of HMG rats. Data are presented as mean ± standard deviation (mean ± SD) (n=3). Statistical analysis was performed using one-way ANOVA. ***P < 0.001, compared with the control group; #P < 0.05, ##P < 0.01, ###P < 0.001, compared with the model group. Detailed Implementation

[0015] To facilitate understanding of the present invention, a more complete description will be provided below. The present invention can be implemented in many different forms and is not limited to the embodiments described herein. Rather, these embodiments are provided to provide a thorough and complete understanding of the disclosure of the present invention.

[0016] Unless otherwise specified, experimental methods in the following examples are generally performed under standard conditions or as recommended by the manufacturer. All commonly used chemical reagents used in the examples are commercially available products.

[0017] Unless otherwise defined, all technical and scientific terms used in this invention have the same meaning as commonly understood by one of ordinary skill in the art to which this invention pertains. The terminology used in this specification is for the purpose of describing particular embodiments only and is not intended to limit the invention. The term "and / or" as used in this invention includes any and all combinations of one or more of the associated listed items.

[0018] Furthermore, as used herein, the term "or" is an inclusive "or" sign and is equivalent to the term "and / or" unless the context clearly specifies otherwise. The term "based on" is not exclusive and allows for basing on other factors not described unless the context clearly specifies otherwise. Additionally, throughout the specification, the meanings of "an," "a," and "the" include plural indicators. The meaning of "in" includes both "in" and "on."

[0019] Some embodiments of the present invention relate to the use of S-propyne cysteine ​​or a pharmaceutically acceptable salt thereof in the preparation of medicaments for improving or treating breast hyperplasia.

[0020] Some embodiments of the present invention relate to the use of S-propyne cysteine ​​or a pharmaceutically acceptable salt thereof in the preparation of medicaments for improving or treating breast hyperplasia complicated with depression.

[0021] This invention demonstrates the therapeutic effect of SPRC on mammary hyperplasia complicated with chronic stress in rats by constructing a rat model. Experimental results show that SPRC significantly improves depressive-like behaviors in the model rats, manifested as increased sucrose preference, shortened immobility time in the forced swimming test, and increased swimming and struggling time. Simultaneously, SPRC effectively inhibits estrogen-induced breast enlargement, reduces nipple diameter and height, and alleviates pathological changes in mammary tissue, including a reduction in the number of ductal epithelial cell layers and alveoli. At the molecular level, SPRC downregulates serum inflammatory factors (IL-6, IL-1, TNF-α), regulates sex hormone-related indicators (such as E2, FSH, PRL), and inhibits the expression of estrogen receptor (ER), progesterone receptor (PR), and proliferating cell nuclear antigen (PCNA) proteins in mammary tissue. Furthermore, SPRC reduces the overexpression of gonadotropin-releasing hormone (GnRH) in the hypothalamus and inhibits the activation of the PI3K-AKT signaling pathway (manifested as a decrease in p-AKT protein levels). These experimental data demonstrate that SPRC can effectively alleviate breast hyperplasia and its associated chronic stress-induced depressive-like behaviors by regulating neuroendocrine, inflammatory responses and proliferation-related signaling pathways through multiple targets. This indicates that SPRC can be used to prepare drugs for the treatment of breast hyperplasia, especially breast hyperplasia-related diseases accompanied by chronic stress or depression.

[0022] In some embodiments of the present invention, the S-propyne cysteine ​​or a pharmaceutically acceptable salt thereof can downregulate the levels of serum inflammatory factors IL-6, IL-1 and TNF-α in patients with breast hyperplasia or breast hyperplasia complicated with depression.

[0023] In some embodiments of the present invention, the S-propynylcysteine ​​or a pharmaceutically acceptable salt thereof can downregulate the E2 and PRL hormone levels in patients with breast hyperplasia or breast hyperplasia complicated with depression, and upregulate the FSH hormone levels in patients with breast hyperplasia or breast hyperplasia complicated with depression.

[0024] In some embodiments of the present invention, the S-propynylcysteine ​​or a pharmaceutically acceptable salt thereof can inhibit the expression of estrogen receptor protein, progesterone receptor protein and proliferating cell nuclear antigen protein in the breast tissue of patients with breast hyperplasia or breast hyperplasia complicated with depression.

[0025] In some embodiments of the present invention, the S-propynylcysteine ​​or a pharmaceutically acceptable salt thereof can reduce the expression of gonadotropin-releasing hormone in the hypothalamus of patients with breast hyperplasia or breast hyperplasia complicated with depression.

[0026] In some embodiments of the present invention, the S-propyne cysteine ​​or a pharmaceutically acceptable salt thereof can reduce p-AKT protein levels in patients with breast hyperplasia or breast hyperplasia complicated with depression.

[0027] In some embodiments of the present invention, the S-propynylcysteine ​​or a pharmaceutically acceptable salt thereof can inhibit the activation of the PI3K-AKT signaling pathway in patients with breast hyperplasia or breast hyperplasia complicated with depression.

[0028] In some embodiments of the present invention, the S-propynylcysteine ​​or a pharmaceutically acceptable salt thereof can reduce the number of ductal epithelial cell layers and alveoli in the breast tissue of patients with breast hyperplasia or breast hyperplasia complicated with depression.

[0029] In some embodiments of the present invention, the drug uses S-propargylcysteine ​​or a pharmaceutically acceptable salt thereof as the active ingredient, and further includes pharmaceutically acceptable excipients, which include one or more of flavoring agents, suspending agents, buffers, binders, diluents, disintegrants, lubricants, solubilizers, thickeners, and fillers.

[0030] The present invention will be further described in detail below with reference to specific embodiments.

[0031] In the following experiments, SPRC refers to S-propargylcysteine, whose structural formula is:

[0032]

[0033] Example 1: Sucrose water preference and forced swimming experiment

[0034] 1. Laboratory animals and grouping

[0035] Fifty SPF-grade female SD rats (6-8 weeks old, weighing 180-200g) were randomly divided into a normal control group (10 rats) and a mammary hyperplasia model group (40 rats) after 1 week of acclimatization feeding.

[0036] Mammary hyperplasia modeling: In the model group, rats were alternately injected with estradiol benzoate (0.5 mg / kg / d, once daily for 25 days) into the hind leg muscles. From day 26 onwards, progesterone (5 mg / kg / d, once daily for 5 days) was administered. After the last progesterone injection, estradiol benzoate (0.5 mg / kg / d) was injected every 2 days to maintain estrogen levels. The normal control group was injected with an equal volume of physiological saline.

[0037] 2. Modeling of chronic stress

[0038] During the modeling of mammary hyperplasia, rats in the model group were housed in solitary cages and subjected to unpredictable chronic stress stimulation (including: 24 hours of 45° inclined cage, 6 hours of restraint, 40 minutes of shaking, 20 hours of wet mat, 24 hours of water deprivation, 24 hours of fasting, and nighttime lighting). Stimulation was administered once daily for the first 30 days and once every other day for the following 30 days, with the stimulation sequence randomized to avoid adaptation. In this invention, rats modeled with estrogen injection combined with chronic stress stimulation are referred to as HMG rats.

[0039] 3. Dosing regimen

[0040] After successful modeling, 10 rats in the normal control group and the model control group were intraperitoneally injected with 10 mL / kg of physiological saline, while rats in the drug groups were intraperitoneally injected with SPRC at doses of 10 mg / kg, 20 mg / kg, and 40 mg / kg (each dose group consisted of 10 rats with mammary hyperplasia). During the drug administration period, the diameter and height of the left nipple of the rats were measured using calipers.

[0041] 4. Sucrose water preference experiment

[0042] Experiments were conducted after model establishment, 15 days after drug administration, and 30 days after drug administration. Before the experiment, students underwent water acclimatization training (first two bottles of 1% sucrose solution for 24 hours, then one bottle of sucrose solution plus one bottle of purified water for 24 hours). After fasting and abstaining from water for 14-23 hours, one bottle each of 1% sucrose solution and purified water were administered simultaneously. One hour later, the students were weighed and their sucrose craving was calculated. Sucrose craving (%) = (Sucrose solution consumption / Total fluid consumption) × 100%.

[0043] 5. Forced swimming test

[0044] The experiments were conducted after model establishment and 30 days after drug administration. A glass tank (50 cm × 30 cm × 60 cm) was used, with a water depth of 30 cm and a water temperature of 25 ± 1℃. One day before the experiment, students swam for 15 minutes, and 24 hours later, they swam for 5 minutes. The duration of immobility, swimming, and climbing behaviors within 5 minutes and the immobility latency were recorded and analyzed.

[0045] 6. Experimental Results and Analysis

[0046] After estrogen injection combined with chronic stress stimulation to establish the model, the rats in the model group showed breast enlargement, proliferative changes in mammary tissue, prolonged immobility time in the forced swimming test, and decreased sucrose water preference, indicating successful model establishment.

[0047] Depend on Figure 1 As shown in Table 1, SPRC treatment significantly increased the sucrose preference of the model rats, significantly shortened the immobility time in the forced swimming test, and significantly increased the swimming time and struggling time. This demonstrates that SPRC can significantly improve depressive-like behavior in a rat model of mammary hyperplasia with chronic stress.

[0048] Table 1. Effects of forced swimming test on depressive behavior in rats with mammary hyperplasia.

[0049]

[0050] All results are expressed as mean ± standard deviation (mean ± SD), (n = 10). Statistical analysis was performed using one-way ANOVA. **p < 0.01 vs. control group, #p < 0.05, ##p < 0.01 vs. model group.

[0051] Figure 2 (A) shows the changes in nipple height in rats of different groups at different time points. Figure 2 (B) shows the changes in nipple diameter at different time points in each group of rats. After estrogen injection, the breasts of the model group animals were significantly enlarged, with both breast diameter and nipple height significantly increased compared to the normal group. SPRC can inhibit estrogen-induced breast enlargement and significantly reduce breast diameter and nipple height.

[0052] Example 2: Effects of SPRC on sex hormone and inflammatory factor levels in HMG rats

[0053] After modeling and administration of the drug as described in Example 1 for 30 days, the rats were sacrificed, and rat serum was extracted. The changes in sex hormone levels and inflammatory factors in the serum of HMG rats were detected using relevant ELISA kits.

[0054] The results are shown in Table 2: Each SPRC dose group exhibited a certain inhibitory effect on inflammatory factors (IL-6, IL-1) and also regulated the sex hormone axis (especially E2, FSH, and PRL), with some indicators showing dose-related changes. Chronic stress activates the hypothalamus-pituitary-adrenal axis, inhibiting gonadotropin-releasing hormone secretion and leading to hypothalamic-pituitary-gonadal axis dysfunction, manifested as decreased follicle-stimulating hormone (FSH) and abnormally elevated estradiol (E2) and prolactin (PRL). Simultaneously, it activates the immune system, upregulating inflammatory factors such as interleukin-6, interleukin-1β, and tumor necrosis factor-α. Elevated estradiol and prolactin synergistically drive mammary epithelial cell proliferation, while inflammatory factors further induce local estradiol synthesis, forming a vicious cycle of "inflammation-hormones," ultimately promoting mammary hyperplasia. SPRC can simultaneously reduce the levels of estradiol, prolactin, and inflammatory factors, and restore the level of follicle-stimulating hormone, indicating that it exerts a dual effect of treating breast hyperplasia and alleviating depressive-like behavior by regulating the neuro-endocrine-immune network in the central nervous system (hypothalamus).

[0055] Table 2. Expression of sex hormones and inflammatory factors in serum of HMG rats after SPRC treatment.

[0056]

[0057] All results are expressed as mean ± standard deviation (mean ± SD), (n = 10). Statistical analysis was performed using one-way ANOVA. *p < 0.05, **p < 0.01 vs. control group, #p < 0.05, ##p < 0.01 vs. model group.

[0058] Example 3: Effects of SPRC on mammary gland tissue of HMG rats

[0059] (1) After modeling and administration of the drug according to the method in Example 1 for 30 days, the rats were sacrificed, and the second pair of intact mammary gland tissues were taken, embedded in paraffin, sectioned, stained with hematoxylin and eosin (HE), and the morphological changes of the mammary gland tissues of each group of rats were observed under an optical microscope. Stereometry was performed on the mammary lobules and acini and ducts in the lobules of each group of rats, and different fields of view were taken from each pathological section for counting.

[0060] Figure 3 The results in Table 3 show that, compared with the blank control group, the number of ductal epithelial cell layers in the model group was significantly increased; compared with the model group, SPRC dose-dependently decreased the number of ductal epithelial cell layers. Compared with the blank control group, the number of acinar cells in the model group increased significantly (P<0.01); compared with the model group, SPRC dose-dependently decreased the number of acinar cells.

[0061] Table 3

[0062]

[0063] All results are expressed as mean ± standard deviation (mean ± SD), (n = 10). Statistical analysis was performed using one-way ANOVA. **p < 0.01 vs. control group, ##p < 0.01 vs. model group.

[0064] (2) After modeling and administration according to the method in Example 1 for 30 days, rats were sacrificed, and rat mammary gland tissue was collected, fixed with 4% paraformaldehyde, embedded in paraffin, and sectioned (4 μm). The sections were dewaxed to water, and antigen retrieval was performed (sodium citrate buffer, high-pressure retrieval), endogenous peroxidase was inactivated with 3% hydrogen peroxide, and blocked with 5% goat serum. Anti-ER, anti-PR, and anti-PCNA primary antibodies (dilution ratios of 1:200, 1:200, and 1:400, respectively) were added and incubated overnight at 4°C; the corresponding secondary antibodies were added the next day, DAB staining was performed, and hematoxylin counterstaining was performed.

[0065] Figure 4The results showed that the proportion of estrogen receptor (ER) protein-positive area and the mean optical density (IOD) in the mammary tissue of the model group rats were significantly increased, indicating that the mammary tissue was more sensitive to estrogen and in a state of hyperestrogen response. Simultaneously, the expression levels of progesterone receptor (PR) and proliferating cell nuclear antigen (PCNA) proteins were also significantly increased. After SPRC intervention, ER protein expression in all dose groups was lower than that in the model group, showing a dose-dependent trend; PR and PCNA protein expression were also synchronously downregulated. ER downregulation can reduce the sensitivity of mammary tissue to estrogen and block proliferative signals; synchronous PR downregulation further weakens the synergistic proliferative effect of progesterone; and PCNA reduction directly confirms the inhibition of abnormal cell proliferation.

[0066] Example 4: Effect of SPRC on Gonadotropin-Releasing Hormone (GnRH) Protein Expression in HMG Rats

[0067] After 30 days of modeling and drug administration as described in Example 1, rats were sacrificed, and hypothalamic tissue was collected. The tissue was fixed in 4% paraformaldehyde, embedded in paraffin, and sectioned (4 μm). Sections were dewaxed to water and subjected to antigen retrieval (sodium citrate buffer, high-pressure retrieval). Endogenous peroxidase was inactivated with 3% hydrogen peroxide, and the sections were blocked with 5% goat serum. Rabbit anti-rat GnRH primary antibody (1:200 dilution) was added and incubated overnight at 4°C. The next day, the corresponding secondary antibody was added, followed by DAB staining and hematoxylin counterstaining. Five fields of view were randomly selected from each section, and the percentage of positively stained area and the average optical density (IOD) were measured using an image analysis system.

[0068] Figure 5 The results in Table 4 show that, compared with the blank control group, the positive expression of gonadotropin-releasing hormone (GnRH) protein in the hypothalamic tissue of rats in the model group was significantly enhanced, as evidenced by an increase in the positive staining area and a deeper staining. Quantitative analysis showed a significant increase in the proportion of positive area, suggesting hyperfunction of the central neuroendocrine system in the model group. Compared with the model group, the positive expression of GnRH protein in each SPRC dose group showed a decreasing trend after intervention, indicating that it can inhibit the overexpression of GnRH in the hypothalamus to a certain extent, thereby regulating the function of the hypothalamus-pituitary-gonadal axis (HPO axis).

[0069] Table 4

[0070]

[0071] All results are expressed as mean ± standard deviation (mean ± SD), (n = 10). Statistical analysis was performed using one-way ANOVA. *p < 0.05 vs. control group, #p < 0.05 vs. model group.

[0072] Example 5: Effect of SPRC on p-AKT protein expression in HMG rats

[0073] After modeling and drug administration as described in Example 1 for 30 days, rats were sacrificed, and mammary gland tissue from each group was collected. Total protein was extracted using RIPA lysis buffer, and protein concentration was determined by the BCA method. Equal amounts of protein (30 μg / well) were separated by SDS-PAGE gel electrophoresis and transferred to PVDF membranes. The membranes were blocked with 5% skim milk powder at room temperature for 1 h, and rabbit anti-rat p-AKT primary antibody (dilution ratio 1:1000) and internal control GAPDH antibody (1:5000) were added, followed by incubation at 4°C overnight. After washing, HRP-labeled goat anti-rabbit secondary antibody (1:5000) was added, and the membranes were incubated at room temperature for 1 h, followed by ECL chemiluminescence imaging. ImageJ software was used to analyze the band gray values, and the relative expression level of p-AKT was expressed as the gray ratio of p-AKT to β-Actin.

[0074] Figure 6 The changes in p-AKT protein in HMG rats after SPRC treatment are shown. (A) is a Western Blot plot, and (B) is the relative expression level of p-AKT. The results demonstrate that SPRC can treat mammary hyperplasia by inhibiting the PI3K-AKT pathway.

[0075] The embodiments described above are merely illustrative of several implementations of the present invention, and while the descriptions are relatively specific and detailed, they should not be construed as limiting the scope of the invention patent. It should be noted that those skilled in the art can make various modifications and improvements without departing from the concept of the present invention, and these all fall within the protection scope of the present invention. Therefore, the protection scope of this invention patent should be determined by the appended claims.

Claims

1. The use of S-propynylcysteine ​​or a pharmaceutically acceptable salt thereof in the preparation of medicaments for improving or treating breast hyperplasia.

2. The use of S-propynylcysteine ​​or a pharmaceutically acceptable salt thereof in the preparation of medicaments for improving or treating breast hyperplasia complicated with depression.

3. The application according to claim 1 or 2, characterized in that, The S-propynylcysteine ​​or its pharmaceutically acceptable salt can downregulate the levels of serum inflammatory factors IL-6, IL-1, and TNF-α in patients with breast hyperplasia or breast hyperplasia complicated with depression.

4. The application according to claim 1 or 2, characterized in that, The S-propynylcysteine ​​or its pharmaceutically acceptable salt can downregulate estradiol and prolactin levels in patients with breast hyperplasia or breast hyperplasia complicated with depression, and upregulate follicle-stimulating hormone levels in patients with breast hyperplasia or breast hyperplasia complicated with depression.

5. The application according to claim 1 or 2, characterized in that, The S-propynylcysteine ​​or its pharmaceutically acceptable salt can inhibit the expression of estrogen receptor protein, progesterone receptor protein, and proliferating cell nuclear antigen protein in the breast tissue of patients with breast hyperplasia or breast hyperplasia complicated with depression.

6. The application according to claim 1 or 2, characterized in that, The S-propynylcysteine ​​or its pharmaceutically acceptable salt can reduce the expression of gonadotropin-releasing hormone in the hypothalamus of patients with breast hyperplasia or breast hyperplasia complicated with depression.

7. The application according to claim 1 or 2, characterized in that, The S-propynylcysteine ​​or its pharmaceutically acceptable salt can reduce p-AKT protein levels in patients with breast hyperplasia or breast hyperplasia complicated with depression.

8. The application according to claim 1 or 2, characterized in that, The S-propynylcysteine ​​or its pharmaceutically acceptable salt can inhibit the activation of the PI3K-AKT signaling pathway in patients with breast hyperplasia or breast hyperplasia complicated with depression.

9. The application according to claim 1 or 2, characterized in that, The S-propynylcysteine ​​or its pharmaceutically acceptable salt can reduce the number of ductal epithelial cell layers and alveoli in the breast tissue of patients with breast hyperplasia or breast hyperplasia complicated with depression.

10. The application according to claim 1 or 2, characterized in that, The drug uses S-propynylcysteine ​​or a pharmaceutically acceptable salt thereof as its active ingredient, and also includes pharmaceutically acceptable excipients, which include one or more of flavoring agents, suspending agents, buffers, binders, diluents, disintegrants, lubricants, solubilizers, thickeners, and fillers.

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