Application of ZIF-8 (at) TG in preparation of medicine or combined medicine for preventing and treating muscular atrophy related diseases

Abstract

The invention discloses application of ZIF-8 at TG in preparation of a medicine or a combined medicine for preventing and treating muscular atrophy related diseases, and belongs to the field of biomedicine.The ZIF-8 at TG has the effect of delaying muscular atrophy induced by nerve injury and delaying reduction of muscular functions and quality of hind limbs of mice and reduction of the cross-sectional area of muscle fibers caused by the nerve injury, and the ZIF-8 at TG has the function of delaying muscular atrophy induced by the nerve injury and also has the function of delaying muscular atrophy induced by the nerve injury and the function of delaying muscular atrophy induced by the nerve injury. The ZIF-8 at TG emphasizes that ZIF-8 and tectorigenin exert a synergistic effect, and finally exerts an effect of delaying muscle atrophy induced by nerve injury.

Description

Technical Field

[0001] The present invention belongs to the field of biomedicine technology, and specifically relates to an application of ZIF-8@TG in the preparation of a drug or a combination drug for preventing and treating diseases related to muscle atrophy. Background Art

[0002] With the development of society and the advancement of science and technology, people's demand for health is growing. Nerve damage is a common clinical condition that can lead to severe muscle atrophy and dysfunction. Muscle atrophy, especially muscle atrophy caused by nerve damage, not only seriously affects the patient's physical health, but also affects the patient's mental health and social interaction ability. At present, the methods for treating muscle atrophy mainly include drug therapy, physical therapy and surgical treatment, but these methods have certain limitations, such as limited therapeutic effect, complicated treatment process, and large side effects of surgical treatment. To date, the treatment of muscle atrophy is still an unresolved problem. Exercise therapy is a relatively effective method for treating skeletal muscle atrophy, but exercise is not suitable for all patients, such as bedridden patients with nerve damage and fracture patients. Therefore, there is an urgent need to develop new drugs or combination drugs to prevent and treat muscle atrophy-related diseases.

[0003] Muscular atrophy induced by nerve damage is mainly due to the obstruction of nerve signal transmission, which causes the muscle to lose normal neurotrophic support and then atrophy. This atrophy not only affects the strength and endurance of the muscle, but may also cause changes in the morphology and structure of muscle fibers, affecting the function and appearance of the muscle. The pathogenesis of muscle atrophy is relatively complex, among which oxidative stress, mitochondrial dysfunction, reduced protein synthesis, and enhanced proteolysis play a very important role in muscle atrophy. Among them, the enhancement of proteolysis capacity is mainly activated through the two major pathways of the ubiquitin-proteasome system and the autophagy-lysosome system, thereby promoting the occurrence of muscle atrophy. Muscular atrophy usually leads to the loss of muscle mass and function, which is characterized by reduced cross-sectional area and mass of muscle fibers, increased degradation of muscle proteins, etc. A variety of pathological conditions can cause skeletal muscle atrophy. Therefore, measures to improve the cross-sectional area of ​​muscle fibers and muscle mass can be used to prevent and treat muscle atrophy-related diseases.

[0004] In order to solve the problem of muscle atrophy after nerve injury, the medical community and researchers have been exploring new treatment methods. In recent years, with the development of nanotechnology, smart nano drug delivery systems have shown great potential in the treatment of various diseases due to their advantages such as precise targeting, sustained release control and biocompatibility. As an emerging treatment method, smart nano sustained-release drug systems have attracted much attention due to their unique advantages. Using nanotechnology, drugs are encapsulated in nanocarriers, and the speed and time of drug release are controlled to achieve precise delivery and sustained action of drugs. However, the application of this technology in the treatment of muscle atrophy, especially in the field of muscle atrophy diseases induced by nerve injury, is still in its infancy.

[0005] Tectorigenin (TG), also known as tectorigenin, is an isoflavone compound found in the Iridaceae family, but TG has poor water solubility and fat solubility, and low oral availability. Nanomaterials can improve drug bioavailability, and one of the most representative drug delivery and release carriers is zeolitic imidazolate framework-8 (ZIF-8). ZIF-8 releases zinc ions under inflammatory conditions, exerting anti-inflammatory and antioxidant effects. Based on the superior drug loading and delivery properties of ZIF-8, the inventors successfully constructed ZIF-8 nanoparticles and ZIF-8@TG nano delivery systems loaded with TG. The present application ZIF-8@TG can delay the occurrence of muscle atrophy after nerve injury, significantly improve the function of atrophic muscles after nerve injury, and inhibit the reduction of muscle mass and muscle fiber cross-sectional area. The present application provides an experimental basis for developing ZIF-8@TG intelligent sustained-release nanoparticles as a new drug or combination drug for the prevention and treatment of muscle atrophy-related diseases. Summary of the invention

[0006] Technical issues solved:

[0007] This application aims at the deficiencies of the existing technology and solves the technical problems such as the limited treatment effect of current muscular atrophy-related diseases, the complicated treatment process, and the large side effects of surgical treatment. It provides an application of ZIF-8@TG in the preparation of drugs or combination drugs for the prevention and treatment of muscular atrophy-related diseases.

[0008] Technical solution:

[0009] To achieve the above objectives, this application is implemented through the following technical solutions:

[0010] A use of ZIF-8@TG in the preparation of a drug or a combination drug for preventing and treating diseases related to muscle atrophy, wherein ZIF-8@TG serves as an active ingredient.

[0011] Furthermore, the muscle atrophy-related disease is a disease related to skeletal muscle, cardiac muscle, and smooth muscle.

[0012] Furthermore, the muscle atrophy-related diseases are muscle atrophy associated with decreased muscle mass, weakened muscle function, muscle atrophy after nerve damage, denervation muscle atrophy, disuse muscle atrophy, age-related muscle atrophy, amyotrophic lateral sclerosis, progressive muscular atrophy of the spinal cord, muscular dystrophy, myositis, and sarcopenia.

[0013] Furthermore, the muscle atrophy-related disease is amyotrophic lateral sclerosis associated with diabetes.

[0014] Furthermore, the muscle atrophy-related disease is muscular dystrophy caused by cachexia.

[0015] Furthermore, the dosage range of the ZIF-8@TG is 5 mg to 80 mg per individual body weight (kg).

[0016] Furthermore, the drug or combination drug for preventing and treating muscular atrophy-related diseases is administered orally, intravenously, intramuscularly, transdermally, through the mucosa, intranasally, intratracheally or subcutaneously.

[0017] Furthermore, the drug or combination drug for preventing and treating diseases related to muscle atrophy is administered once a day, once every two days, once every three days, once a week, once a month or once a year during a period from one day to one year.

[0018] Furthermore, the ZIF-8@TG construction steps are:

[0019] Step 1: Add 0.2 mL of 24 mM Zn(NO3)2·6(H2O), 0.2 mL of 1.3 mM 1,2-dimethylimidazole, 5 mL of 100 mM Hepes buffer, and 0.7 mL of 10 mM CTAB into a glass bottle and stir at room temperature to obtain a ZIF-8 solution;

[0020] Step 2: Add 0.3 mL of 500 μg / mL TG solution to the ZIF-8 solution, stir at room temperature until the Tyndall effect is a ZIF-8@TG solution, centrifuge to remove the supernatant, add methanol and deionized water, centrifuge to remove the supernatant, and freeze-dry to obtain ZIF-8@TG nanoparticles.

[0021] Beneficial effects:

[0022] The present application provides an application of ZIF-8@TG in the preparation of a drug or a combination drug for preventing and treating diseases related to muscle atrophy, which has the following beneficial effects compared with the prior art:

[0023] 1. TG was loaded into ZIF-8 to obtain ZIF-8@TG nanoparticles, which showed a rhombic polyhedral morphology with a particle size of about 50-60 nm. The incorporation of TG hardly destroyed the ordered crystalline ZIF-8 framework;

[0024] 2. ZIF-8@TG has the effect of improving the function of atrophic muscles induced by nerve injury. In the experimental study of muscle function in mice after nerve injury, ZIF-8@TG can significantly reduce the heat withdrawal reaction time of mice induced by nerve injury and increase the hanging time on the inverted grid;

[0025] 3. ZIF-8@TG has the effect of delaying muscle atrophy induced by nerve injury. In the experimental study of skeletal muscle of mice with nerve injury, ZIF-8@TG can significantly inhibit the reduction of tibialis anterior muscle weight and body mass index after nerve injury.

[0026] 4. ZIF-8@TG has the effect of improving the reduction of muscle fiber cross-sectional area during muscle atrophy after nerve injury. In the experimental study of skeletal muscle of mice with nerve injury, ZIF-8@TG can significantly inhibit the reduction of tibialis anterior muscle fiber cross-sectional area. BRIEF DESCRIPTION OF THE DRAWINGS

[0027] Figure 1 The experimental results of ZIF-8 and ZIF-8@TG synthesized in this application are shown in the figure; the upper figure is a scanning electron microscope image of ZIF-8, Scale bars: 100nm; the lower figure is a scanning electron microscope image of ZIF-8@TG, Scale bars: 200nm;

[0028] Figure 2 This application shows that ZIF-8@TG can improve the muscle function of mice with nerve crush, where A is the thermal withdrawal reaction time of mice; B is the inverted grid hanging drop time of mice, data are expressed as mean ± standard deviation (n≥3), *P<0.05, **P<0.01, ***P<0.001, ns: no significant difference;

[0029] Figure 3 The present application shows that ZIF-8@TG can inhibit the atrophy of the tibialis anterior muscle after nerve injury in mice, wherein Figure A is the weight of the tibialis anterior muscle of mice; Figure B is the ratio of the weight of the tibialis anterior muscle of mice to body weight, data are expressed as mean ± standard deviation (n≥3), *P<0.05, **P<0.01, ***P<0.001, ns: no significant difference;

[0030] Figure 4This is a graph of the reduction in muscle fiber cross-sectional area during muscle atrophy after nerve injury inhibited by ZIF-8@TG in this application, specifically the cross-sectional area of ​​mouse tibialis anterior muscle fibers. The data are expressed as mean ± standard deviation (n≥3), *P<0.05, **P<0.01, ***P<0.001. DETAILED DESCRIPTION

[0031] The present invention will be described below in conjunction with specific embodiments. The described embodiments are only a part of the embodiments of the present invention rather than all of them, and these embodiments are only used to illustrate the present invention and are not used to limit the protection scope of the present invention, which is defined by the claims.

[0032] The experimental methods described in the following examples are conventional methods unless otherwise specified; the reagents and biological materials described are commercially available unless otherwise specified.

[0033] Iridogenin TG (HPLC ≥ 98%) was purchased from Chengdu Purifa Technology Development Co., Ltd.

[0034] Embodiment 1:

[0035] Due to the limitations of TG molecular structure, its water solubility and fat solubility are poor, and its oral availability is not high. In order to improve the application of TG and give full play to the pharmacological effect of TG in inhibiting muscular atrophy, this application selects ZIF-8 as the nanocarrier for the best delivery and release of TG. In view of this, this application first constructs ZIF-8 and ZIF-8@TG sustained-release nanoparticles.

[0036] A use of ZIF-8@TG in preparing a drug or a combination drug for preventing and treating diseases related to muscle atrophy, specifically comprising the following steps:

[0037] Step 1: Add Zn(NO3)2·6(H2O) (24mM, 0.2mL), 1,2-dimethylimidazole (2-mel, 1.3mM, 0.2mL), Hepes buffer (pH 7.4, 100mM, 5mL), and CTAB (10mM, 0.7mL) into a glass bottle, stir at room temperature to obtain a ZIF-8 solution, remove the supernatant after centrifugation, add methanol and deionized water, remove the supernatant after centrifugation, and freeze-dry to obtain ZIF-8 nanoparticles;

[0038] Step 2: Add TG solution (500 μg / mL, 0.3 mL) to ZIF-8 solution, stir at room temperature until the Tyndall effect is ZIF-8@TG solution, centrifuge to remove the supernatant, add methanol and deionized water, centrifuge to remove the supernatant, and freeze-dry to obtain ZIF-8@TG nanoparticles. The morphological characteristics of the synthesized ZIF-8 and ZIF-8@TG were observed using SEM.

[0039] like Figure 1 As shown, ZIF-8 nanoparticles have a distinct rhombic dodecahedral structure, which is consistent with the typical morphology of ZIF-8 reported in the literature ( Figure 1 ZIF-8@TG nanoparticles have a rhombic polyhedron-like morphology with a particle size of about 50-60 nm ( Figure 1 Lower middle figure), indicating the successful construction of ZIF-8 and ZIF-8@TG nanoparticles.

[0040] Embodiment 2:

[0041] Effects of ZIF-8@TG on motor function of mice with skeletal muscle atrophy induced by nerve injury:

[0042] Skeletal muscle plays a vital role in important activities such as exercise. After nerve damage, skeletal muscle loses its contractile function, resulting in reduced protein synthesis and increased proteolysis in target muscles, which ultimately leads to weakened motor function and muscle atrophy. In view of this, this application first explores the effect of ZIF-8@TG nanoparticles on the motor function of muscular atrophy mice induced by nerve damage.

[0043] Materials and animals: Iridogenin (HPLC ≥ 98%) was purchased from Chengdu Prefa Technology Development Co., Ltd.; 8-week-old male ICR mice (SPF grade) were provided by the Experimental Animal Center of Nantong University.

[0044] Methods: ICR mice were randomly divided into control group (Control group), sciatic nerve crush group (Crush group), tectoriusin treatment group after sciatic nerve crush (TG group), ZIF-8 treatment group after sciatic nerve crush (ZIF-8 group) and ZIF-8@TG treatment group after sciatic nerve crush (ZIF-8@TG group). Sciatic nerve crush was performed by intraperitoneal injection of mouse anesthetic (1.25% Avertin, 0.2mL / 10g), shaving the fur on the outer side of the left thigh of the mouse with a shaver and disinfecting the skin. An oblique incision was made on the outer side of the mouse thigh, and the thigh muscles were bluntly separated with ophthalmic scissors. The left sciatic nerve was fully exposed and clamped with hemostatic forceps (3 times, 10s each time). After surgery, the wound was sutured and disinfected routinely. After sciatic nerve crush, mice were intraperitoneally injected with control solvent, 5 mg / kg TG (irisin was dissolved in DMSO and diluted with saline, and the proportion of DMSO did not exceed 1%), 40 mg / kg ZIF-8 (ZIF-8 was dissolved in DMSO and diluted with saline, and the proportion of DMSO did not exceed 1%), and 40 mg / kg ZIF-8@TG (ZIF-8@TG was dissolved in DMSO and diluted with saline, and the proportion of DMSO did not exceed 1%) every three days. The mice were tested for motor function 18 days after surgery.

[0045] The method of the heat pain withdrawal test is as follows: Use a hot plate analgesia instrument to induce pain, accurately adjust the temperature of the hot plate to about 50°C, and calibrate it with a mercury thermometer. After the mouse is stable, put it on the hot stage, and record the time when the mouse quickly raises its paw, shakes, licks, retracts or even jumps after the heat stimulation. The cutoff time is 30 seconds to prevent burns.

[0046] The inverted grid test method is as follows: using an elevated inverted wire grid test, the ability of mice to stably grasp the grid is utilized to assess neuromuscular strength and coordination, and the time it takes for mice to fall from the grid is recorded.

[0047] Results: Figure 2 As shown, compared with the control group (Control), the heat pain withdrawal reaction time of the sciatic nerve injured mice (Crush) was significantly increased ( Figure 2 A) and the inverted grid suspension residence time is significantly reduced ( Figure 2 Middle B), the increase in thermal pain withdrawal reaction time in mice treated with ZIF-8 (ZIF-8) was inhibited ( Figure 2 Middle A), the increase in thermal pain withdrawal reaction time and the decrease in inverted grid hanging residence time of mice in the ZIF-8@TG treatment group (ZIF-8@TG) were also significantly inhibited ( Figure 2 ), and was superior to the TG group and the ZIF-8 group, indicating that ZIF-8 and irisin played a synergistic role, and the muscle function impairment induced by nerve injury was significantly improved after ZIF-8@TG treatment.

[0048] Embodiment 3:

[0049] Effects of ZIF-8@TG on the tibialis anterior muscle of mice with skeletal muscle atrophy induced by nerve injury:

[0050] Skeletal muscle atrophy is characterized by a decrease in muscle mass. In view of this, the present application investigates the effect of ZIF-8@TG nanoparticles on the tibialis anterior muscle weight and body mass index of mice with muscular atrophy induced by nerve injury.

[0051] Materials and animals: Iridogenin (HPLC ≥ 98%) was purchased from Chengdu Prefa Technology Development Co., Ltd.; 8-week-old male ICR mice (SPF grade) were provided by the Experimental Animal Center of Nantong University.

[0052] Methods: ICR mice were randomly divided into control group (Control group), sciatic nerve crush group (Crush group), tectoriusin treatment group after sciatic nerve crush (TG group), ZIF-8 treatment group after sciatic nerve crush (ZIF-8 group) and ZIF-8@TG treatment group after sciatic nerve crush (ZIF-8@TG group). Sciatic nerve crush was performed by intraperitoneal injection of mouse anesthetic (1.25% Avertin, 0.2mL / 10g), shaving the fur on the outer side of the left thigh of the mouse with a shaver and disinfecting the skin. An oblique incision was made on the outer side of the mouse thigh, and the thigh muscles were bluntly separated with ophthalmic scissors. The left sciatic nerve was fully exposed and clamped with hemostatic forceps (3 times, 10s each time). After surgery, the wound was sutured and disinfected routinely. After sciatic nerve crush, mice were intraperitoneally injected with control solvent, 5 mg / kg TG (irisin was dissolved in DMSO and diluted with normal saline, and the proportion of DMSO did not exceed 1%), 40 mg / kg ZIF-8 (ZIF-8 was dissolved in DMSO and diluted with normal saline, and the proportion of DMSO did not exceed 1%), and 40 mg / kg ZIF-8@TG (ZIF-8@TG was dissolved in DMSO and diluted with normal saline, and the proportion of DMSO did not exceed 1%) every three days. After 18 days, the mice were weighed, and the tibialis anterior muscles were sampled and weighed.

[0053] The calculation method of the tibialis anterior muscle weight index is as follows: the mouse is weighed, the tibialis anterior muscle is sampled and weighed, and the weight of the tibialis anterior muscle on the injured side is divided by the weight of the mouse to obtain the tibialis anterior muscle weight index.

[0054] Results: Figure 3 As shown, compared with the control group (Control), the tibialis anterior muscle weight of sciatic nerve injured mice (Crush) ( Figure 3 A) and tibialis anterior muscle mass index ( Figure 3 B) was significantly decreased, while the tibialis anterior muscle weight of mice in the ZIF-8@TG treatment group (ZIF-8@TG) was Figure 3 A) and tibialis anterior muscle mass index ( Figure 3 The decrease of B) was inhibited and was better than that of TG group and ZIF-8 group.

[0055] Embodiment 4:

[0056] Effect of ZIF-8@TG on the cross-sectional area of ​​tibialis anterior muscle fibers in mice with skeletal muscle atrophy induced by nerve injury:

[0057] Skeletal muscle atrophy is characterized by a decrease in the cross-sectional area of ​​muscle fibers. In view of this, the present application investigates the effect of ZIF-8@TG nanoparticles on the cross-sectional area of ​​tibialis anterior muscle fibers in mice with muscular atrophy induced by nerve injury.

[0058] Materials and animals: Iridogenin (HPLC ≥ 98%) was purchased from Chengdu Prefa Technology Development Co., Ltd.; anti-laminin antibody (Cat. No. ab11575) and Donkey Anti-Rabbit IgG H&L (Alexa 488) antibody was purchased from Abcam. 8-week-old male ICR mice (SPF grade) were provided by the Experimental Animal Center of Nantong University.

[0059] Methods: ICR mice were randomly divided into control group (Control group), sciatic nerve crush group (Crush group), tectoriusin treatment group after sciatic nerve crush (TG group), ZIF-8 treatment group after sciatic nerve crush (ZIF-8 group) and ZIF-8@TG treatment group after sciatic nerve crush (ZIF-8@TG group). Sciatic nerve crush was performed by intraperitoneal injection of mouse anesthetic (1.25% Avertin, 0.2mL / 10g), shaving the fur on the outer side of the left thigh of the mouse with a shaver and disinfecting the skin. An oblique incision was made on the outer side of the mouse thigh, and the thigh muscles were bluntly separated with ophthalmic scissors. The left sciatic nerve was fully exposed and clamped with hemostatic forceps (3 times, 10s each time). After surgery, the wound was sutured and disinfected routinely. After sciatic nerve crush, mice were intraperitoneally injected with control solvent, 5 mg / kg TG (irisin was dissolved in DMSO and diluted with normal saline, the proportion of DMSO did not exceed 1%), 40 mg / kg ZIF-8 (ZIF-8 was dissolved in DMSO and diluted with normal saline, the proportion of DMSO did not exceed 1%), and 40 mg / kg ZIF-8@TG (ZIF-8@TG was dissolved in DMSO and diluted with normal saline, the proportion of DMSO did not exceed 1%) every three days. The tibialis anterior muscles of mice were collected 18 days after surgery.

[0060] The immunohistochemical staining method is as follows: Cut the middle section of the tibialis anterior muscle into cross sections and fix them in 4% paraformaldehyde solution at 4°C for 24 hours, then dehydrate them in 10% sucrose, 20% sucrose, and 30% sucrose solutions every 12 hours. After embedding the muscle tissue with OCT, use a freezing microtome to make 10μm sections and bake them in a 37°C oven overnight. Wash with PBS three times, 5 minutes each time. First, block with blocking solution at room temperature for 2 hours, add anti-laminin antibody and incubate at 4°C overnight. Wash the sections with PBS for 10 minutes and wash three times. Then add DonkeyAnti-Rabbit IgG H&L (Alexa The slides were incubated with 488) antibody at room temperature in the dark for 2 h. The slides were washed with PBS for 10 min and three times. The slides were then sealed with DAPI-containing sealing solution, and the fluorescence images of the tibialis anterior muscle were captured with a Zeiss fluorescence microscope. The muscle fiber cross-sectional area of ​​the obtained images was measured using ImageJ software.

[0061] Results: Figure 4As shown, the results of laminin staining of the tibialis anterior muscle showed that compared with the control group (Control), the muscle fiber area of ​​the tibialis anterior muscle of the sciatic nerve injured mice (Crush) was significantly reduced, indicating obvious atrophy; the decrease in the muscle fiber area of ​​the tibialis anterior muscle of the ZIF-8 treated group (ZIF-8) mice was inhibited, and at the same time, the ZIF-8@TG treated group

[0062] The decrease in muscle fiber area of ​​the tibialis anterior muscle of (ZIF-8@TG) mice was significantly inhibited, and was superior to that of the TG group and the ZIF-8 group.

[0063] These results indicate that ZIF-8 and irisinogenin exert synergistic effects, and nerve injury-induced muscle atrophy is significantly improved after ZIF-8@TG treatment.

[0064] The present invention is described above by way of example. It should be noted that, without departing from the core of the present invention, any simple deformation, modification or other equivalent replacement that can be made by those skilled in the art without inventive effort falls within the protection scope of the present invention.

Claims

1. A use of ZIF-8@TG in the preparation of a drug or a combination drug for preventing and treating diseases related to muscle atrophy, characterized in that: ZIF-8@TG as the active ingredient.

2. The use of ZIF-8@TG according to claim 1 in the preparation of a drug or a combination drug for preventing and treating diseases related to muscle atrophy, characterized in that: The muscle atrophy-related diseases are diseases related to skeletal muscle, cardiac muscle, and smooth muscle.

3. The use of ZIF-8@TG according to claim 1 in the preparation of a drug or a combination drug for preventing and treating diseases related to muscle atrophy, characterized in that: The muscle atrophy-related diseases are muscle atrophy associated with decreased muscle mass, weakened muscle function, muscle atrophy after nerve damage, denervation muscle atrophy, disuse muscle atrophy, age-related muscle atrophy, amyotrophic lateral sclerosis, progressive muscular atrophy of the spinal cord, muscular dystrophy, myositis, and sarcopenia.

4. The use of ZIF-8@TG according to claim 1 in the preparation of a drug or a combination drug for preventing and treating diseases related to muscle atrophy, characterized in that: The muscle wasting-related disease is diabetic-related amyotrophy.

5. The use of ZIF-8@TG according to claim 1 in the preparation of a drug or a combination drug for preventing and treating diseases related to muscle atrophy, characterized in that: The muscle wasting-related disease is muscular dystrophy caused by cachexia.

6. The use of ZIF-8@TG according to claim 1 in the preparation of a drug or a combination drug for preventing and treating diseases related to muscle atrophy, characterized in that: The dosage range of the ZIF-8@TG is 5 mg to 80 mg per individual body weight (kg).

7. The use of ZIF-8@TG according to claim 1 in the preparation of a drug or a combination drug for preventing and treating diseases related to muscle atrophy, characterized in that: The drug or combination drug for preventing and treating muscular atrophy-related diseases is administered orally, intravenously, intramuscularly, transdermally, through the mucosa, intranasally, intratracheally or subcutaneously.

8. The use of ZIF-8@TG according to claim 1 in the preparation of a drug or a combination drug for preventing and treating diseases related to muscle atrophy, characterized in that: The drug or combination drug for preventing and treating diseases related to muscle atrophy is administered once a day, once every two days, once every three days, once a week, once a month or once a year during a period from one day to one year.

9. The use of ZIF-8@TG in the preparation of a drug or a combination drug for preventing and treating diseases related to muscle atrophy according to claim 1, characterized in that: The ZIF-8@TG construction steps are: Step 1: Add 0.2 mL of 24 mM Zn(NO3)2·6(H2O), 0.2 mL of 1.3 mM 1,2-dimethylimidazole, 5 mL of 100 mM Hepes buffer, and 0.7 mL of 10 mM CTAB into a glass bottle and stir at room temperature to obtain a ZIF-8 solution; Step 2: Add 0.3 mL of 500 μg / mL TG solution to the ZIF-8 solution, stir at room temperature until the Tyndall effect is a ZIF-8@TG solution, centrifuge to remove the supernatant, add methanol and deionized water, centrifuge to remove the supernatant, and freeze-dry to obtain ZIF-8@TG nanoparticles.

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