Application of deaminotyrosine in improvement or prevention and treatment of muscle atrophy

Abstract

The invention discloses application of deaminotyrosine in improvement or prevention and treatment of muscular atrophy, and relates to the technical field of biological medicines. The invention finds that in the cellular level, DAT can effectively resist C2C12 myoblast senescence induced by etoposide; in a dexamethasone-induced C2C12 myotube atrophy model, DAT not only inhibits myotube diameter reduction from the form, but also down-regulates mRNA expression of key atrophy genes Atrogin-1 and MuRF-1 from the molecular level, and inhibits excessive activation of a ubiquitin-proteasome system; in-vivo animal experiments prove that DAT can reverse aging-related dyskinesia of rapidly-aged SAMP8 mice, and gait parameters of the rapidly-aged SAMP8 mice are all remarkably improved. According to the invention, a complete evidence chain from cells to the whole is constructed, and the DAT is proved to improve the senescent skeletal muscle atrophy through multiple ways of intervening cell senescence, antagonizing protein degradation, improving muscle microenvironment and the like, and shows important potential application value.

Description

Technical Field

[0001] This invention belongs to the field of biomedical technology, specifically relating to the application of deaminotyrosine in improving or preventing muscle atrophy. Background Technology

[0002] Skeletal muscle is not only a core component of the body's musculoskeletal system but also a vital organ for maintaining metabolic homeostasis. With the increasing aging of the global population, age-related skeletal muscle atrophy (also known as sarcopenia) has become an increasingly serious public health problem. Sarcopenia is characterized by progressive muscle loss, decreased muscle strength, and functional decline, severely leading to mobility impairments, increased risk of falls, deterioration of quality of life, and increased mortality in the elderly.

[0003] Currently, clinical interventions for age-related muscle atrophy are extremely limited, primarily relying on nutritional support (such as protein and vitamin D supplementation) and resistance training. However, these basic interventions have limited effectiveness for frail elderly individuals, and adherence is difficult to guarantee. In the field of drug development, although the academic community has been exploring treatments that directly target muscle metabolic pathways, no breakthrough progress has been achieved to date. For example, some studies have attempted to promote muscle growth by modulating the myostatin pathway, activating AKT / mTOR synthesis signaling, or inhibiting degradation pathways such as ubiquitin-proteasome, but these strategies often face significant challenges such as poor target specificity, large systemic side effects, or unknown long-term safety. Therefore, developing a safe, effective, and easily marketable anti-aging muscle atrophy drug is a core issue that urgently needs to be addressed in this field.

[0004] In recent years, research on the relationship between gut microbiota and host health, particularly with the aging process, has provided a novel perspective for the treatment of metabolic diseases. Deaminated tyrosine (DAT, source leaf S31303), a natural aromatic amino acid metabolite produced by gut microbes from dietary fiber metabolism, has gradually come into the research spotlight. Existing technologies have preliminarily revealed various biological activities of DAT. For example, published research reports have confirmed that DAT, as an endogenous agonist of hydroxycarboxylic acid receptor 3 (HCAR3 / GPR109a), possesses potent anti-inflammatory and antioxidant effects, effectively alleviating tissue damage in cardiovascular disease models such as myocardial ischemia-reperfusion injury and atherosclerosis. In addition, studies have also shown that DAT can exert neuroprotective effects in the nervous system and participate in regulating the body's glucose and lipid metabolism homeostasis.

[0005] However, existing technologies still have the following obvious defects and insufficient understanding: (1) Limited research scope: Existing research on DAT is highly concentrated in the fields of cardiovascular, nervous system and basal metabolism, and its application is generally limited to these categories. Existing technologies have not addressed the role of DAT in the skeletal muscle system, especially in the major age-related disease of muscle atrophy, nor have they provided any technical insights. (2) One-sided understanding of the mechanism of action: Existing technologies only recognize the basic effects of DAT, such as systemic anti-inflammatory effects, but completely ignore its potential value in regulating the gut-muscle axis communication, acting directly on skeletal muscle cells, coordinating the balance of protein synthesis and degradation, and improving the function of muscle stem cells. This narrow understanding of the biological functions of DAT seriously limits its development prospects as a muscle-targeted therapy drug. (3) Disconnection from the treatment of age-related muscle atrophy: Although chronic inflammation and oxidative stress are recognized as the core mechanisms driving aging and muscle atrophy, existing technologies have never linked DAT, a natural molecule with ideal anti-inflammatory and antioxidant properties, with the clear technical need for anti-muscle aging. There is a huge technical gap between the two.

[0006] Whether DAT can directly intervene in skeletal muscle mass and function, and its clear "gut-muscle axis" connection, remains an important unresolved scientific gap. Because the significant efficacy of DAT in the aforementioned related fields has been proven, systematically exploring its relationship with muscle atrophy is not only theoretically necessary, but also holds promise for opening up a new direction for combating sarcopenia using endogenous metabolites as an intervention strategy. Summary of the Invention

[0007] Against this backdrop, the present invention breaks through the bottleneck of existing anti-muscle atrophy drug development by innovatively discovering that the natural metabolite deaminotyrosine can effectively alleviate skeletal muscle atrophy caused by aging. It opens up a new direction for combating sarcopenia by using endogenous metabolites as an intervention strategy, and provides a new scientific strategy for addressing the challenges of aging and achieving "healthy aging".

[0008] To achieve the above objectives, the present invention adopts the following technical solution: One objective of this invention is to provide the use of deaminotyrosine in the preparation of products that improve and / or prevent muscle atrophy.

[0009] A second objective of this invention is to provide the use of compositions containing deaminotyrosine in the preparation of products that improve and / or prevent muscle atrophy.

[0010] Furthermore, the product type can be any one of pharmaceuticals, health products, functional foods, and dietary supplements.

[0011] Furthermore, the drug also includes a pharmaceutically acceptable carrier.

[0012] Furthermore, the pharmaceutically acceptable carrier is any one or more of the following: diluent, binder, antioxidant, pH adjuster, preservative, lubricant, and disintegrant.

[0013] Furthermore, the dosage form of the drug is any one of capsules, tablets, microcapsules, injections, suppositories, sprays, and ointments.

[0014] Furthermore, the drug can be administered via injection, oral administration, inhalation spray, or transdermal delivery.

[0015] Furthermore, the muscle atrophy includes age-related muscle atrophy.

[0016] Furthermore, the product exerts its effect of improving and / or preventing muscle atrophy through any one or more of the following pathways: (1) Delay the aging process of myogenic cells; (2) Antagonizes induced myotube atrophy; (3) Improve the motor function of aging bodies; (4) Regulates the gene network related to muscle tissue fibrosis and atrophy.

[0017] Compared with the prior art, the present invention has the following significant advantages and outstanding technological progress: 1. Originality and target novelty: This invention reveals and verifies for the first time the novel pharmaceutical use of the natural metabolite deaminotyrosine (DAT) in the prevention and improvement of age-related skeletal muscle atrophy. It breaks through the existing research boundaries that limit the application of DAT to the cardiovascular and metabolic fields, and provides a new, safe candidate molecule and unique target for the development of anti-muscle aging drugs.

[0018] 2. Multi-level and synergistic mechanism of action: This invention confirms that DAT does not exert its effects through a single pathway, but rather through a multi-level and synergistic mechanism of action involving "anti-cellular senescence + inhibition of protein degradation + improvement of motor function + reversal of fibrosis + reshaping of cell differentiation trajectory". This comprehensive protective effect from the molecular, cellular, to the whole animal level can more effectively reverse the complex pathological process of muscle aging compared to a single-target strategy.

[0019] 3. Potential for source intervention and disease modification: Unlike simply supplementing nutrition or passively fighting inflammation, this invention demonstrates through cutting-edge technologies such as single-cell sequencing that DAT can "reset" the tissue state of aging muscles to a younger and healthier differentiation trajectory at the level of cell fate, showing its great potential as a disease modification therapy, rather than just symptomatic treatment.

[0020] 4. Natural source and high safety: DAT is an endogenous intestinal flora metabolite in the human body, which exists in the human metabolic pathway. Therefore, compared with completely exogenous synthetic drugs, the intervention method provided by this invention is expected to have natural advantages such as good biocompatibility, low risk of side effects, and high tolerance to the body, making it particularly suitable for long-term use by the elderly.

[0021] 5. Broad application prospects: This invention not only lays a solid foundation for the development of prescription drugs for the treatment of age-related muscle atrophy (sarcomustia), but also provides clear scientific basis for the development of functional foods or dietary supplements for the daily health care of middle-aged and elderly people and to delay muscle decline. The market application prospects are extremely broad. Attached Figure Description

[0022] The accompanying drawings, which are included to provide a further understanding of the invention and form part of this invention, illustrate exemplary embodiments of the invention and are used to explain the invention, but do not constitute an undue limitation of the invention. In the drawings: Figure 1 This is the verification process of DAT directly delaying the senescence process of myogenic cells in Example 1 of the present invention, including the detection results of cell senescence degree and senescence-related protein expression in each treatment group in the etoposide-induced C2C12 myoblast senescence model.

[0023] Figure 2 The verification process for the effective antagonism of DAT against induced myotube atrophy in Example 1 of this invention includes the immunofluorescence staining results of each treatment group in the dexamethasone-induced C2C12 myotube atrophy model, the myotube morphology analysis results, and the qPCR detection results of the expression of key genes for muscle atrophy.

[0024] Figure 3 This is the verification process of DAT improving the motor function of aging mice in vivo in Example 1 of the present invention, including the evaluation results of relevant gait parameters of each treatment group in the aging model mice.

[0025] Figure 4 The verification process for DAT improving muscle tissue fibrosis and inhibiting muscle atrophy in Example 1 of the present invention includes Masson staining results and Western Blot analysis results of each treatment group in aging model mice. Detailed Implementation

[0026] The following examples are used to illustrate the present invention, but are not intended to limit the scope of the invention. Any modifications or substitutions made to the methods, steps, or conditions of the present invention without departing from the spirit and essence of the invention are within the scope of the invention. The reagents, products, and instruments used in the following examples are all commercially available, and the methods used in the examples, unless otherwise specified, are consistent with conventional methods.

[0027] This invention, by integrating in vitro cell models, ex vivo organ culture, and in vivo animal experiments, constructs a multi-level, comprehensive chain of evidence, fully demonstrating the significant effect and clear mechanism of deaminotyrosine (DAT) in improving age-related skeletal muscle atrophy. The specific technical solution is as follows: (1) DAT directly delays the aging process of myogenic cells. In in vitro experiments, this invention used an etoposide-induced C2C12 myoblast senescence model. Quantitative analysis using SA-β-galactosidase senescence staining showed that, compared to the model group, the DAT-treated group (preferably at a concentration of 50-200 μM) exhibited a significantly reduced SA-β-galactosidase-positive cell rate. Furthermore, Western blot analysis demonstrated that DAT effectively upregulated the expression levels of the senescence-related protein p21 and the DNA damage marker H2ax. These results represent the first cellular-level demonstration that DAT possesses direct efficacy against myogenic cell senescence.

[0028] (2) DAT effectively antagonizes induced myotube atrophy To simulate muscle atrophy, this invention intervened in a dexamethasone-induced C2C12 myotube atrophy model. Immunofluorescence staining was used to quantitatively measure myotube diameter, revealing that DAT treatment significantly inhibited the dexamethasone-induced decrease in myotube diameter. Furthermore, qPCR detection showed that DAT significantly downregulated the mRNA expression levels of key muscle atrophy markers Atrogin-1 and MuRF-1. This experiment demonstrates that DAT not only morphologically alleviates myotube atrophy but also inhibits the overactivation of the ubiquitin-proteasome system at the molecular level.

[0029] (3) DAT improves motor function in aging mice in vivo This invention uses the rapidly aging SAMP8 mouse model for in vivo experiments. After 8 weeks of intervention with DAT (preferred dose 150 mM / L daily, administered via water) in aging mice, the mice's voluntary movements were quantitatively assessed using a high-precision gait analysis system. The results clearly showed that, compared with the untreated aging control group, the DAT-treated mice exhibited significant improvements in stride length, stride distance, and swing speed. Simultaneously, parameters reflecting support stability, such as paw print area and standing time, were also significantly enhanced. This indicates that DAT can effectively improve age-related motor dysfunction and restore the animals' motor coordination and strength.

[0030] (4) DAT regulates the gene network related to muscle tissue fibrosis and atrophy. RNA was extracted from the anterior tibialis muscle of mice, and qPCR and MASSON staining analysis of tissue sections revealed that DAT significantly reversed the abnormally high expression of pro-fibrosis genes in aging muscles. Simultaneously, Western blot results showed that DAT treatment inhibited the expression of muscle atrophy-related factors Murf-1 and Atrogin-1, and regulated the expression of a series of genes related to the balance between muscle protein synthesis and degradation, collectively creating a molecular environment conducive to maintaining muscle mass.

[0031] The technical solution of the present invention will be further described in detail below with reference to the embodiments. Example

[0032] (1) Validation experiment on DAT directly delaying the aging process of myogenic cells In in vitro experiments, this invention uses an etoposide-induced C2C12 myoblast senescence model to verify that DAT directly delays the senescence process of myogenic cells.

[0033] ① C2C12 cells (ATCC, CBP60252) were routinely cultured in DMEM high-glucose medium containing 10% fetal bovine serum and placed in an incubator at 37℃ and 5% CO2. The experiment was divided into the following groups: A: Control group: normally cultured cells. B: Model group: cells treated with 5 μM etoposide for 48 hours to induce cell senescence. C: DAT treatment group: in addition to the model group, cells were treated with 100 μM and 200 μM DAT (Yuan Ye, S31303) for intervention.

[0034] ② Cell senescence assay (SA-β-galactosidase staining): After drug treatment, discard the culture medium and wash the cells twice with PBS. Follow the instructions for the SA-β-galactosidase staining kit, adding fixative and staining working solution. Incubate at 37°C in a CO2-free incubator for 16 hours in the dark. Observe under a regular optical microscope and take pictures of multiple randomly selected fields of view. Count the number of SA-β-galactosidase-positive cells showing blue color and calculate the positive cell rate. The experiment was independently repeated three times.

[0035] ③ Detection of aging-related protein expression (Western Blot): After drug treatment, cells were washed with pre-cooled PBS, lysed on ice with RIPA lysis buffer, and total protein was collected. Protein concentration was determined and quantified using the BCA method. SDS-PAGE electrophoresis was performed, and the protein was transferred to a PVDF membrane. After blocking with 5% skim milk, diluted primary antibodies (p21, H2ax, and internal control GAPDH) were added, and the membrane was incubated overnight at 4°C. The next day, the membrane was washed with TBST, and the corresponding HRP-labeled secondary antibodies were added and incubated at room temperature for 1 hour. Developing was performed using an ECL chemiluminescence kit, and images were acquired in a gel imaging system. The gray values ​​of each protein band were analyzed using ImageJ software, and semi-quantitative analysis was performed using the ratio of target protein to internal control GAPDH.

[0036] ④ Experimental results ( Figure 1 ): SA-β-galactosidase staining: Compared with the control group, the blue positive cell rate was significantly increased in the model group. Compared with the model group, the positive cell rate in each DAT treatment group (especially the 100 μM and 200 μM concentrations) showed a significant dose-dependent decrease.

[0037] Western blot analysis showed that the protein expression levels of p21 and H2ax were significantly upregulated in the model group cells. The DAT treatment group effectively reversed this trend, significantly downregulating the protein expression levels of p21 and H2ax.

[0038] This result is the first time that DAT has demonstrated at the cellular level its efficacy in directly combating myogenic cellular senescence.

[0039] (2) Verification experiment on the effectiveness of DAT in antagonizing induced myotube atrophy This experiment aims to verify the antagonistic effect of deaminotyrosine (DAT) on dexamethasone-induced C2C12 myotube atrophy in vitro and to provide evidence from both morphological and molecular biological perspectives.

[0040] ① Myotube differentiation and experimental grouping: C2C12 cells were cultured in growth medium (DMEM containing 10% FBS) to approximately 80% confluence, and then replaced with differentiation medium (DMEM containing 2% horse serum) to induce differentiation into myotubes. The differentiation process lasted 5-7 days, with fresh differentiation medium replaced every 24 hours until a large number of multinucleated mature myotubes were formed.

[0041] ② The experiment was set up with the following groups: Control group: Mature myotubes, cultured normally.

[0042] Model group: 100 μM dexamethasone was added to the differentiation medium and treated for 48 hours to induce myotube atrophy.

[0043] DAT treatment group: 100 μM DAT was added to the differentiation medium containing 100 μM dexamethasone and the intervention lasted for 48 hours.

[0044] ③ Immunofluorescence staining and myotube morphological analysis: After drug treatment, the culture medium was discarded, and the cells were gently washed twice with PBS. Cells were fixed with 4% paraformaldehyde for 15 minutes, followed by permeabilization with 0.1% Triton X-100 for 10 minutes. After blocking with 5% BSA at room temperature for 1 hour, anti-myosin heavy chain (myoG) primary antibody was added, and the cells were incubated overnight at 4°C. The next day, after washing with PBS, the cells were incubated with the appropriate fluorescently labeled secondary antibody (e.g., Alexa Fluor 488-labeled goat anti-mouse IgG) at room temperature in the dark for 1 hour. The cell nuclei were counterstained with DAPI for 5 minutes. Images were captured using a confocal fluorescence microscope. At least 10 fields of view were randomly selected from each sample, and the diameter of at least 100 myotubes was measured using ImageJ software, followed by statistical analysis.

[0045] ④ qPCR detection of expression of key genes for muscle atrophy: After drug treatment, total RNA was extracted from cells in each group directly using TRIzol reagent. After determining RNA concentration and purity, 1 μg of total RNA was reverse transcribed into cDNA using a reverse transcription kit. Using cDNA as a template, real-time quantitative PCR was performed using SYBR Green premixed buffer and specific primers (Atrogin-1, MuRF-1, and the internal control gene Actin). The reaction program was: 95℃ pre-denaturation for 30 seconds; 95℃ for 5 seconds, 60℃ for 30 seconds, for a total of 40 cycles. The relative expression levels of Atrogin-1 and MuRF-1 mRNA were calculated using the 2^(-ΔΔCt) method.

[0046] ⑤ Experimental results ( Figure 2 ): Immunofluorescence staining: Compared with the control group, the myotube structure in the dexamethasone model group was significantly thinner, and the myotube diameter was significantly reduced. In contrast, compared with the model group, the myotube diameter in the DAT treatment group was significantly maintained, and the morphology was thicker and healthier.

[0047] qPCR analysis: In the dexamethasone model group, the mRNA expression levels of Atrogin-1 and MuRF-1 were significantly upregulated compared to the control group. DAT treatment, however, significantly downregulated the gene expression of these two key E3 ubiquitin ligases in a dose-dependent manner.

[0048] (3) Validation experiment on DAT's improvement of motor function in aging mice in vivo In vivo experiments were conducted using the rapidly aging SAMP8 mouse model. After 8 weeks of intervention with deaminotyrosine (DAT) (preferred dose 150 mM / L daily, administered via water), the spontaneous movement of the mice was quantitatively assessed using a high-precision gait analysis system. The aim was to validate, at the whole-animal level, the ameliorative effect of long-term DAT supplementation on motor dysfunction in the rapidly aging SAMP8 mouse model.

[0049] ① Laboratory Animals and Feeding: Six-month-old male SAMP8 mice were used (at this age, significant age-related decline in muscle function and motor coordination has begun; Jiangsu Huachuang Xinno Pharmaceutical Technology Co., Ltd. http: / / www.jshcxn.com / proinfo / 15.html). Simultaneously, the same-age, genetically similar anti-aging SAMR1 mouse strain was used as a normal aging control. All mice were housed under specific pathogen-free conditions, maintained a 12-hour light-dark cycle, and had free access to standard laboratory feed. All animal experimental procedures followed the guidelines of the Institutional Animal Care and Use Committee.

[0050] ② Experimental grouping and drug administration regimen: Groups: A: Normal aging control group (SAMR1 group): SAMR1 mice, with free access to ordinary sterilized water. B: Aging model control group (SAMP8-CTRL group): SAMP8 mice, with free access to ordinary sterilized water. C: DAT treatment group (SAMP8-DAT group): SAMP8 mice, with free access to sterilized water containing 1.5 mM DAT.

[0051] ③ DAT was administered via drinking water for 8 weeks. Freshly prepared DAT aqueous solution was administered twice weekly, and the daily DAT intake was estimated to be approximately 150 mg / kg / day by measuring the mice's water intake and body weight. This administration method is non-invasive and long-lasting, effectively mimicking the scenario of long-term dietary supplementation.

[0052] ④ Motor Function Assessment (Gait Analysis) Assessment Time: Conducted after 8 weeks of intervention. A high-precision small animal gait analysis system was used. Mice were allowed to walk autonomously on a transparent walking track equipped with a top-mounted high-speed camera. The soles of the mice's paws were coated with different colors of non-toxic ink to leave clear paw prints on the walking paper. At least 3 consecutive, stable walking cycles were recorded for each mouse. The gait dynamic parameters of the mice were analyzed: stride length, stride distance, and swing speed. All data are expressed as mean ± standard error. Statistical software was used, and one-way ANOVA combined with post-hoc tests (such as Tukey's test) was employed for comparisons among multiple groups. A p < 0.05 was considered statistically significant.

[0053] ⑤ Experimental results ( Figure 3Compared with the SAMP8 group, mice in the SAMP8-DAT group showed significant improvement in all gait parameters after 8 weeks of intervention.

[0054] (4) Validation experiment on the gene network related to DAT regulation of muscle tissue fibrosis and atrophy This experiment aims to verify the inhibitory effect of DAT on the fibrosis process of skeletal muscle in aging mice from the perspectives of tissue morphology and molecular level, and to explore its specific regulatory role in key pathways of muscle atrophy.

[0055] ① The experimental materials were derived from mice euthanized after 8 weeks of intervention in the above experiment. The quadriceps femoris (QU) muscle was used as the sampling site, as this muscle is susceptible to damage in aging and neuromuscular diseases and is sensitive to pathological changes. Groups: normal control group (SAMR1 group), aging model control group (SAMP8 group), and DAT treatment group (SAMP8-DAT group).

[0056] ② Experimental Methods: Tissue Sectioning and Masson's Trichrome Staining: Tissue Fixation and Embedding: Partial tibialis anterior muscle tissue was taken, fixed in 4% paraformaldehyde for 24 hours, and then routinely embedded in paraffin. The paraffin block was serially sectioned to a thickness of 5 μm. The Masson's trichrome staining kit was strictly followed according to the instructions. Under an optical microscope, muscle fibers were stained red, and collagen fibers were stained blue. Five non-overlapping fields of view were randomly selected from each group. Image-Pro Plus or ImageJ software was used to calculate the percentage of blue collagen fiber area in each field of view, i.e., collagen volume fraction (CVF), and statistical analysis was performed.

[0057] ③ Western Blot: Protein extraction: Approximately 50 mg of tibialis anterior muscle tissue was ground into powder in liquid nitrogen and lysed on ice using RIPA lysis buffer (containing protease inhibitors and phosphatase inhibitors). Protein concentration was determined using the BCA method. An equal volume of protein was subjected to SDS-PAGE electrophoresis. The protein was transferred to a PVDF membrane and blocked with 5% skim milk for 1 hour. The membrane was incubated overnight at 4°C with specific primary antibodies. Target primary antibodies included MuRF-1 and Atrogin-1, with GAPDH as an internal control. After incubation with HRP-labeled secondary antibodies at room temperature for 1 hour, the membrane was developed using ECL chemiluminescence reagent. Images were acquired using a chemiluminescence imaging system, and the gray values ​​of the target bands were analyzed using ImageJ software. Semi-quantitative analysis was performed using the ratio of target protein to internal control.

[0058] ④ Experimental results ( Figure 4 ): Masson staining: Compared with the SAMR1 group, the SAMP8-CTRL group showed a large amount of blue collagen fiber deposition in muscle tissue, and a significantly increased CVF. Compared with the SAMP8-CTRL group, the blue area in the SAMP8-DAT group was significantly reduced, and the CVF was significantly decreased.

[0059] Western blot analysis showed that the protein expression levels of MuRF-1 and Atrogin-1 in muscle tissue of the SAMP8-CTRL group were significantly upregulated. DAT intervention, on the other hand, significantly downregulated the protein expression of these two key E3 ubiquitin ligases.

[0060] The embodiments described above are merely preferred embodiments of the present invention and are not intended to limit the scope of the present invention. Various modifications and improvements made by those skilled in the art to the technical solutions of the present invention without departing from the spirit of the present invention should fall within the protection scope defined by the claims of the present invention.

Claims

1. Use of desaminotyrosine in the preparation of a product for improving and / or preventing muscle atrophy.

2. Use of a composition comprising desaminotyrosine in the preparation of a product for improving and / or preventing muscle atrophy.

3. The use according to any one of claims 1 to 2, characterized in that, The product type is any one of a drug, a health product, a functional food, and a dietary supplement.

4. Use according to claim 3, characterized in that, The drug further comprises a pharmaceutically acceptable carrier.

5. Use according to claim 4, characterized in that, The pharmaceutically acceptable carrier is any one or more of a diluent, a binder, an antioxidant, a pH regulator, a preservative, a lubricant, and a disintegrant.

6. Use according to claim 4, characterized in that, The dosage form of the drug is any one of a capsule, a tablet, a microcapsule preparation, an injection, a suppository, a spray, and an ointment.

7. Use according to claim 4, characterized in that, The administration mode of the drug is any one of injection, oral administration, inhalation spray, and transdermal administration.

8. Use according to claim 3, characterized in that, The muscle atrophy includes senile muscle atrophy.

9. Use according to claim 8, characterized in that, The product exerts the effect of improving and / or preventing muscle atrophy through any one or more of the following pathways: (1) delaying the aging process of myogenic cells; (2) antagonizing induced myotube atrophy; (3) improving the exercise function of an aging body; (4) regulating the muscle tissue fibrosis and atrophy-related gene network.

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