A traditional Chinese medicine composition for treating neuromuscular junction diseases, a preparation method thereof and application thereof

Abstract

The application discloses a traditional Chinese medicine composition preparation for treating neuromuscular junction diseases and a preparation method and application thereof, and relates to the technical field of medicine and health. The preparation is prepared from the following raw materials in a proportion by weight: 5-30 parts of Camelthorn, 5-30 parts of aloe, 5-30 parts of asafetida, 5-30 parts of mukhallat, 5-30 parts of agastache, 5-30 parts of mustard, 5-30 parts of box fruit vine root and 5-100 parts of Terminalia chebula. The application further provides a preparation method of the preparation, which comprises the steps of extracting, concentrating and drying medicinal materials in water. The composition preparation has a significant curative effect on improving myasthenia symptoms, increasing urine output, protecting neurons and inhibiting neuroinflammation. The preparation has the treatment advantages of multiple targets and multiple pathways, and can be used for preparing medicines for preventing and / or treating neuromuscular junction diseases such as myasthenia gravis and neurogenic bladder.

Description

Technical Field

[0001] This invention relates to the field of medical and health technology, and in particular to a Uyghur medicine composition for treating neuromuscular junction diseases, its preparation method, and its application. Background Technology

[0002] The neuromuscular junction (NMJ) is a complex chemical synapse responsible for transmitting action potentials generated by motor neurons to skeletal muscle fibers, thus executing the muscle contraction command. Neuromuscular junction diseases, such as myasthenia gravis (MG) and neurogenic bladder (NB), are characterized by impaired signal transmission at the NMJ, leading to a range of clinical symptoms including skeletal muscle weakness and difficulty urinating.

[0003] Myasthenia gravis is an acquired autoimmune disease primarily mediated by autoantibodies targeting the postsynaptic membrane acetylcholine receptor (AChR), leading to a decrease in the number and impaired function of AChRs at the NMJ. The global prevalence is on the rise, with an annual incidence of approximately 20-475 cases per million people. Clinical manifestations mainly include skeletal muscle weakness, ptosis (drooping eyelid), and difficulty swallowing; severe cases can lead to myasthenic crisis, which is life-threatening. Current Western medical treatment mainly relies on cholinesterase inhibitors, immunosuppressants, and glucocorticoids, but these treatments suffer from unstable efficacy, significant side effects, and long treatment durations.

[0004] Neurogenic bladder is an abnormal bladder function caused by damage or dysfunction of the nervous system. Diabetic neurogenic bladder (DNB) is one of the most common types, accounting for 40% to 60% of diabetic complications. Its core pathology lies in neuropathy and detrusor muscle dysfunction caused by long-term hyperglycemia. Clinical manifestations include difficulty urinating and urinary retention, severely impacting patients' quality of life. Current clinical treatments are limited, mainly relying on intermittent catheterization or cholinergic drugs, but the efficacy is unstable and systemic side effects exist.

[0005] Neuroinflammation is a common pathological feature of many neuromuscular junction diseases, and excessive inflammatory responses can lead to neuronal damage and synaptic structure disruption. Therefore, finding multi-target drugs that can simultaneously repair neuromuscular junction structures, regulate immune inflammatory responses, and protect neurons is of great significance for the treatment of neuromuscular junction diseases. Summary of the Invention

[0006] The purpose of this invention is to provide a Uyghur medicine composition for treating neuromuscular junction diseases, its preparation method, and its application, thereby addressing the problems existing in the prior art.

[0007] To achieve the above objectives, the present invention provides the following solution: This invention provides a Uyghur medicine composition for treating neuromuscular junction diseases, the composition comprising the following raw materials in parts by weight: 5-30 parts of camel bud, 5-30 parts of aloe vera, 5-30 parts of asafoetida, 5-30 parts of myrrh, 5-30 parts of patchouli, 5-30 parts of mustard seed, 5-30 parts of twig root, and 5-100 parts of chebula.

[0008] Furthermore, the preparation contains the following raw materials in parts by weight: 20 parts of camel bud, 20 parts of aloe vera, 20 parts of asafoetida, 20 parts of myrrh, 20 parts of patchouli, 20 parts of mustard seed, 20 parts of twig root, and 100 parts of chebula.

[0009] Furthermore, the Uyghur medicine composition formulation also includes a pharmaceutically acceptable carrier; the dosage form is capsule, tablet, granule, pill or powder.

[0010] This invention also provides a method for preparing a Uyghur medicine composition for treating neuromuscular junction diseases, comprising the following steps: (1) Weigh out the processed camel buds, patchouli, mustard seeds, box fruit vine roots, and Terminalia chebula according to the weight proportions; (2) Add water to the medicinal materials obtained in step (1) to extract, filter, and obtain the extract; (3) Concentrate the extract obtained in step (2) and dry it to obtain the extract powder; (4) The extract powder obtained in step (3) is mixed with asafoetida, aloe vera, myrrh and pharmaceutically acceptable excipients to prepare a Uyghur medicine composition preparation.

[0011] Furthermore, the extraction in step (2) is a decoction extraction, which is performed 2 to 3 times, with each extraction lasting 1 to 3 hours, and the amount of water added each time being 8 to 15 times the total weight of the medicinal materials.

[0012] Furthermore, the concentration in step (3) is vacuum concentration, the temperature is 50~70℃, and the vacuum degree is -0.075~-0.095MPa; the drying is spray drying or vacuum drying, and the moisture content of the dried powder is ≤5.0%.

[0013] Furthermore, in step (4), the pharmaceutically acceptable excipients are selected from one or more of fillers, binders, flow aids, and lubricants.

[0014] The present invention also provides a capsule of Uyghur medicine composition prepared by the above preparation method, wherein the weight ratio of the extract dry powder to microcrystalline cellulose, micronized silica gel and magnesium stearate is 85:12:2:1.

[0015] The present invention also provides the use of the above-mentioned Uyghur medicine composition in the preparation of drugs for the prevention and / or treatment of neuromuscular junction diseases.

[0016] Furthermore, neuromuscular junction disorders include myasthenia gravis or neurogenic bladder.

[0017] The present invention discloses the following technical effects: The Uyghur medicine composition of this invention can significantly improve the symptoms of myasthenia gravis and repair the neuromuscular junction structure. The Uyghur medicine composition of this invention can effectively reduce the serum acetylcholine receptor antibody (AChR-Ab) level in experimental autoimmune myasthenia gravis (EAMG) rats, significantly enhance the rats' forelimb and whole-body grip strength, prolong suspension time, and reduce Lennon's clinical score, indicating that it can effectively improve myasthenia symptoms. Histopathological and immunofluorescence results show that this preparation can repair damaged gastrocnemius muscle fibers and brain neurons, significantly increase the area and number of acetylcholine receptors (AChR) at the neuromuscular junction (NMJ), and restore the structural integrity of the NMJ.

[0018] The traditional Chinese medicine composition of this invention can effectively alleviate urinary dysfunction in neurogenic bladder and protect nerve tissue: In a rat model of diabetic neurogenic bladder (DNB), the formulation of this invention significantly increased urine output and improved urinary dysfunction. Pathological sections showed that the formulation could reduce bladder mucosal epithelial hyperplasia and smooth muscle hypertrophy, improve neuronal morphology in brain tissue, and promote the repair of myelin sheaths in brain and bladder tissues, indicating that it has a significant protective effect on central and peripheral nerve tissues.

[0019] The Uyghur medicine composition of this invention inhibits neuroinflammatory responses and regulates intracellular calcium homeostasis: In an LPS-induced PC12 cell inflammation model, the formulation of this invention significantly reduced the secretion levels of inflammatory factors TNF-α and IL-6, thus inhibiting neuroinflammatory responses. Simultaneously, this formulation can reduce abnormally elevated intracellular calcium levels. 2+ The concentration of the drug restored calcium homeostasis and reduced cell apoptosis, indicating that it has clear anti-inflammatory and neuroprotective activities.

[0020] This invention exhibits a multi-target synergistic effect with a clearly defined mechanism of action. The formulation of this invention exerts its therapeutic effect by activating the AChR-PLC-MCOLN1-calcium signaling pathway. Western blot and transcriptomic analyses confirmed that the expression levels of AChR, PLC, and MCOLLN1 proteins in rat brain tissue were significantly increased after administration. This formulation, through the synergistic action of multiple components and multiple targets, simultaneously repairs neuromuscular junction structures, regulates immune inflammatory responses, and protects neuronal function, providing a new drug option for the treatment of neuromuscular junction diseases.

[0021] The Uyghur medicine composition of this invention includes camel sedge, aloe vera, asafoetida, myrrh, patchouli, mustard seed, *Heterodendron chinense* root, and chebula. This formula targets facial paralysis, limb muscle weakness, and neurogenic bladder weakness caused by cold stagnation, nerve damage, malnutrition of muscles and viscera, and abnormal bladder qi transformation. It follows the principles of unblocking the meridians and repairing the spirit, nourishing muscles and restoring strength, regulating qi and promoting urination. Camel sedge and mustard seed are the principal herbs. Camel sedge dispels wind and unblocks the meridians, directly reaching the head and face meridians, clearing facial nerve stagnation and improving facial muscle paralysis. Mustard seed is pungent and warm, penetrating the meridians, dispelling cold and opening the orifices, activating relaxed and disused muscle tissue. The two herbs work synergistically to repair damaged nerves, nourish muscles, and restore muscle function, directly addressing the core pathogenesis of facial paralysis and muscle weakness. Mustard seed replaces the toxic watermelon in the original formula, eliminating toxicity while retaining efficacy, significantly improving safety. Terminalia chebula and Ferula assa-foetida serve as adjuvant herbs, their pungent and warm properties dispersing and penetrating deep into the meridians to dispel cold and dampness, assisting the principal herb in unblocking the meridians and nourishing the spirit. Terminalia chebula, used in large quantities, harmonizes Qi, strengthens the meridians, protects the body's vital energy, and moderates the pungent and drying properties of the other herbs, while also consolidating bladder Qi and improving urinary weakness. It is supplemented with the root of the vine of the vine to unblock the meridians, promote urination, and nourish muscles to restore strength; myrrh to invigorate blood circulation, unblock the meridians, and aid in nerve repair; patchouli to promote Qi circulation and clear the meridians; and aloe vera to balance the warming and drying properties of the other herbs and nourish damaged meridians. The entire formula is balanced in its warming and cooling properties, addressing both the root cause and the symptoms, eliminating pathogens without harming the body's vital energy, and unblocking the meridians without damaging them. It repairs damaged nerves, improves muscle relaxation, and regulates bladder function, precisely addressing the treatment needs of facial paralysis, muscle weakness, and urinary weakness caused by nerve damage.

[0022] This formula is a modified version of the classic formula, Aibimantin. The original formula's core ingredient for clearing the meridians was galangal, a proprietary herb in Uyghur medicine used to treat nerve paralysis and cold-induced paralysis. However, due to resource depletion, it is no longer produced in large quantities and cannot be used in modern formulations or clinical applications. Based on Uyghur medical theory and this research, asafoetida and galangal share similar medicinal properties and target the same point. Both are pungent and warm, entering the meridians and excelling at dispersing deep-seated cold, clearing nerve blockages, and repairing meridian damage. Asafoetida can completely replace galangal while retaining the original formula's core efficacy in clearing the meridians and treating paralysis, making it suitable for modern production and safe clinical application. The original formula also includes watermelon, a herb containing medicated ingredients. While this herb has significant effects in clearing the meridians, opening the orifices, and relieving muscle tension and numbness, it is highly toxic, has a narrow therapeutic window, and poses extremely high risks in modern clinical and experimental studies, with serious safety concerns. This formula uses mustard seeds instead of watermelon to precisely retain its core medicinal effects of "pungent and warming to penetrate the meridians, dispel cold and open the orifices, and awaken relaxed muscles," while greatly reducing the toxicity of the original drug. This achieves equivalent efficacy and significantly improves safety, making it more suitable for animal experimental research and long-term clinical application. Attached Figure Description

[0023] To more clearly illustrate the technical solutions in the embodiments of the present invention or the prior art, the drawings used in the embodiments will be briefly introduced below. Obviously, the drawings described below are only some embodiments of the present invention. For those skilled in the art, other drawings can be obtained based on these drawings without creative effort.

[0024] Figure 1 This is a description of the weight changes in rats in Example 6 of the present invention; Figure 2 The AChR-ab and Ca in rats of each group after administration in Example 6 of this invention 2＋ Content detection results; * indicates P<0.05; ** indicates P<0.01; # indicates P<0.05; ## indicates P<0.01; Figure 3 HE slices (200×) of the gastrocnemius muscle of rats in each group of Example 6 of this invention; Figure 4 The cross-sectional area of ​​each rat gastrocnemius muscle unit muscle fiber in Example 6 of this invention; Figure 5 HE-stained sections (200×) of rat brain tissue from each group in Example 6 of this invention. Figure 6 NissL-stained sections (200×) of rat brain tissue from each group in Example 6 of this invention. Figure 7 The image shows the AChR immunofluorescence at the NMJ site of the gastrocnemius muscle in each group of rats in Example 6 of this invention (200×). Figure 8 The image shows the AChR immunofluorescence at the NMJ site in the hind paw of each group of rats in Example 6 of this invention (400×). Figure 9 The following is a description of the acetylcholine receptors at the NMJ in the experimental group rats of Example 6 of this invention; A: area of ​​acetylcholine receptors; B: number of acetylcholine receptors; Figure 10 This refers to the changes in the expression of different proteins in rat tissues in Example 6 of the present invention; Figure 11 This is a differential gene volcano diagram from Example 6 of the present invention; Figure 12 This is a table showing the urine output of rats in Example 7 of the present invention; A: represents the urine output of rats in 12 hours; B: represents the urine output of rats in 2 hours; Compared with the blank group, **P<0.01; Compared with the model group, #P<0.05; ##P<0.01; Figure 13 HE staining images of rat bladders in each group of Example 7 of this invention; Figure 14 HE slices of rat brain tissue from each group in Example 7 of this invention; Figure 15 These are LFB staining images of rat brain tissue from each group in Example 7 of this invention; Figure 16 These are LFB staining images of rat bladder tissue from each group in Example 7 of this invention; Figure 17 Example 8 of this invention illustrates the effect of the formulation of this invention on the proliferation rate of PC12 cells; Figure 18 This is a diagram showing the morphology and apoptosis of PC12 cells in Example 8 of the present invention. Figure 19 The effects of different drug administration groups on Ca in PC12 cells in Example 8 of this invention 2+ The impact of the changes; Figure 20 Example 8 of the present invention illustrates the effect of the formulation of the present invention on the expression of cytokines such as TNF-α and IL-6. Figure 21 This is a description of the weight changes in rats during drug administration in Example 9 of the present invention; Figure 22 The results of whole-body muscle strength measurement in rats in Example 9 of this invention; compared with the blank group, *P<0.05 indicates a significant difference; **P<0.01 indicates a highly significant difference; ns indicates no statistical difference; Figure 23 The results of serum AchR-Ab content determination in Example 9 of this invention; compared with the blank group, *P<0.05 indicates a significant difference; **P<0.01 indicates a highly significant difference; ns indicates no statistical difference; Figure 24 This is a description of the weight changes in rats during drug administration in Example 9 of the present invention; Figure 25 This is a table showing the changes in suspension time of rats in each group after drug administration in Example 9 of the present invention; compared with the blank group, *P<0.05, **P<0.01; compared with the model group, #P<0.05, ##P<0.01; ns indicates no statistical difference; Figure 26 This is a table showing the changes in grip strength of rats in each group after drug administration in Example 9 of the present invention; compared with the blank group, *P<0.05, **P<0.01; compared with the model group, #P<0.05, ##P<0.01; ns indicates no statistical difference; Figure 27 The changes in AchR-ab content in rats in each group after administration in Example 9 of this invention; *P<0.05; **P<0.01; Figure 28 This is a HE-stained section of brain tissue (200×) from Example 9 of the present invention. Figure 29 This is a HE-stained section (200×) of the gastrocnemius muscle tissue from Example 9 of the present invention. Figure 30 This is a Nissl stained section (200×) of brain tissue from Example 9 of the present invention. Detailed Implementation

[0025] Various exemplary embodiments of the present invention will now be described in detail. This detailed description should not be considered as a limitation of the present invention, but rather as a more detailed description of certain aspects, features, and embodiments of the present invention.

[0026] It should be understood that the terminology used in this invention is merely for describing particular embodiments and is not intended to limit the invention. Furthermore, with respect to numerical ranges in this invention, it should be understood that each intermediate value between the upper and lower limits of the range is also specifically disclosed. Any stated value or intermediate value within a stated range, as well as each smaller range between any other stated value or intermediate value within said range, is also included in this invention. The upper and lower limits of these smaller ranges may be independently included or excluded from the range.

[0027] Unless otherwise stated, all technical and scientific terms used herein have the same meaning as commonly understood by one of ordinary skill in the art. While only preferred methods and materials have been described herein, any methods and materials similar or equivalent to those described herein may be used in the implementation or testing of this invention. All references to this specification are incorporated by way of citation to disclose and describe methods and / or materials associated with those references. In the event of any conflict with any incorporated reference, the content of this specification shall prevail.

[0028] Various modifications and variations can be made to the specific embodiments described in this specification without departing from the scope or spirit of the invention, as will be apparent to those skilled in the art. Other embodiments derived from this specification will also be apparent to those skilled in the art. This specification and embodiments are merely exemplary.

[0029] The terms “include,” “including,” “have,” and “contain” used in this article are all open-ended terms, meaning that they include but are not limited to.

[0030] Example 1 A Uyghur medicine composition for treating neuromuscular junction diseases, the preparation method of which includes the following steps: Weigh out 17g of processed camel bud seeds, 17g of agastache, 17g of mustard seeds, 17g of *Heterodactylis praecox* root, and 119g of chebula, and prepare them into a powder. Add 10 times the amount of water to the obtained powder, decoct twice, 1.5 hours each time, filter, and combine the extracts. Concentrate the extract under reduced pressure at 60℃ and -0.08MPa to a fluid extract with a relative density of 1.10~1.15, then vacuum dry, pulverize, and pass through an 80-mesh sieve to obtain a dry extract powder. Take 17g of aloe vera, 17g of asafoetida, and 17g of myrrh, pulverize, pass through an 80-mesh sieve, and mix evenly with the previously prepared dry extract powder to obtain the Uyghur medicine composition of this invention.

[0031] Example 2 A Uyghur medicine composition for treating neuromuscular junction diseases, the preparation method of which includes the following steps: Weigh out 17g of processed camel bud seeds, 17g of agastache, 17g of mustard seeds, 17g of *Heterodactylis praecox* root, and 85g of chebula, and prepare them into a powder. Add 10 times the amount of water to the obtained powder, decoct twice, 1.5 hours each time, filter, and combine the extracts. Concentrate the extract under reduced pressure at 60℃ and -0.08MPa to a fluid extract with a relative density of 1.10~1.15, then vacuum dry, pulverize, and pass through an 80-mesh sieve to obtain a dry extract powder. Take 17g of aloe vera, 17g of asafoetida, and 17g of myrrh, pulverize, pass through an 80-mesh sieve, and mix evenly with the previously prepared dry extract powder to obtain the Uyghur medicine composition of this invention.

[0032] Example 3 A Uyghur medicine composition for treating neuromuscular junction diseases, the preparation method of which includes the following steps: Weigh out 17g of processed camel bud seeds, 17g of agastache, 17g of mustard seeds, 17g of *Heterodactylis praecox* root, and 17g of chebula, and prepare them into a powder. Add 10 times the amount of water to the obtained powder, decoct twice, 1.5 hours each time, filter, and combine the extracts. Concentrate the extract under reduced pressure at 60℃ and -0.075MPa to a fluid extract with a relative density of 1.10~1.15, then vacuum dry, pulverize, and pass through an 80-mesh sieve to obtain a dry extract powder. Take 17g of aloe vera, 17g of asafoetida, and 17g of myrrh, pulverize, pass through an 80-mesh sieve, and mix evenly with the previously prepared dry extract powder to obtain the Uyghur medicine composition of this invention.

[0033] Example 4 A Uyghur medicine composition for treating neuromuscular junction diseases, the preparation method of which includes the following steps: Weigh out 17g of processed camel bud seeds, 17g of patchouli, 17g of mustard seeds, 17g of *Heterodactylis praecox* root, and 340g of *Terminalia chebula*, and prepare them into a powder. Add 15 times the amount of water to the obtained powder, decoct twice, 3 hours each time, filter, and combine the extracts. Concentrate the extract under reduced pressure at 60℃ and -0.095MPa to a fluid extract with a relative density of 1.10~1.15, then vacuum dry, pulverize, and pass through an 80-mesh sieve to obtain a dry extract powder. Take 17g of aloe vera, 17g of asafoetida, and 17g of myrrh, pulverize, pass through an 80-mesh sieve, and mix evenly with the previously prepared dry extract powder to obtain the Uyghur medicine composition powder, which is the Uyghur medicine composition preparation of this invention.

[0034] Example 5 A Uyghur medicine composition capsule for treating neuromuscular junction diseases, the preparation method of which includes the following steps: The Uyghur medicinal composition powder prepared in Example 1 was taken, and its angle of repose was determined to be 32°, with a critical relative humidity of 65%. The dry extract powder was mixed with microcrystalline cellulose (filler), aerosil (glidant) and magnesium stearate (lubricant) at a weight ratio of 85:12:2:1, and mixed uniformly by the equal increment method. The bulk density of the mixed granules was determined to be 0.45 g / mL. Size 0 gelatin capsules were selected, and the theoretical filling amount was calculated based on the total daily powder mass for capsule filling, to obtain the Uyghur medicinal composition capsules.

[0035] Comparative Example 1 A Uyghur medicinal composition preparation was prepared according to the original prescription of Abimanting, and the preparation method comprises the following steps: 17 g of processed Semen Pegani Harmala, 17 g of Colocynth, 17 g of Operculina turpethum root, and 119 g of Fructus Chebulae were weighed and made into medicinal powder. The obtained medicinal powder was added with 10 times the amount of water, decocted and extracted twice for 1.5 hours each time, filtered, and the extract solutions were combined. The extract solution was concentrated under reduced pressure at 60°C and -0.08 MPa to a fluid extract with a relative density of 1.10 to 1.15, then subjected to vacuum drying, pulverization, and sieving through an 80-mesh sieve to obtain dry extract powder; another 17 g of Aloe, 17 g of Asafetida, 17 g of Galbanum, and 17 g of Mukul myrrh were taken, pulverized, sieved through an 80-mesh sieve, and mixed uniformly with the previously prepared dry extract powder, to obtain the Uyghur medicinal composition preparation.

[0036] Example 6 Pharmacodynamic effect and mechanism of Uyghur medicinal composition on experimental autoimmune myasthenia gravis (EAMG) rats 1. Experimental materials 1.1 Experimental animals: SPF grade female SD rats, weighing 170±10 g. Purchased from the Animal Experimental Center of Xinjiang Medical University, with the experimental animal production license number: SCXK (Xin) 2019-0001. The rats were raised in the animal laboratory of Xinjiang Huashidan Pharmaceutical Research Co., Ltd., with a feeding environment at room temperature of 22 to 27°C and a relative humidity of 40% to 60%. All operation procedures in this experiment complied with the regulations of the National Science and Technology Commission for the administration of animal experimental research.

[0037] 1.2 Experimental drugs: The Uyghur medicinal composition preparation prepared in Example 1 of the present invention (hereinafter referred to as "the preparation of the present invention"), and the positive drug prednisone acetate.

[0038] 2. Model establishment, intervention and index detection 2.1 Model establishment: The rat-derived acetylcholine receptor α subunit 97-116 peptide segment (R97-116) multiple immunization method was used to establish the EAMG rat model. The primary, secondary and tertiary immunizations were performed on day 0, day 30 and day 45 respectively.

[0039] 2.2 Grouping and Administration: Rats that successfully developed the model were randomly divided into a model group, a positive drug group (prednisolone acetate, 5.4 mg / kg), and low, medium, and high dose groups of the formulation of this invention (180, 360, and 720 mg / kg), with a normal control group. Each group consisted of 8 rats. The rats were administered the drug via gavage for 28 consecutive days, once daily.

[0040] 2.3 Detection indicators: Lennon clinical score, forelimb and whole-body grip strength, suspension time, serum acetylcholine receptor antibody (AChR-Ab) and calcium ion level; HE and Nissl staining of gastrocnemius muscle and brain tissue; immunofluorescence staining of gastrocnemius muscle and hindfoot acetylcholine receptor (AChR); transcriptomics analysis of brain tissue; Western blot detection of AChR, PLC, and MCOLLN1 protein expression. Results are shown in […]. Figures 1-11 And Tables 1-2.

[0041] 3. Experimental Results 3.1 Effects of the formulation of this invention on behavioral and serological indicators of EAMG rats See the rat weight changes. Figure 1 .like Figure 1 As shown, the body weight of rats in the model group continued to decrease, while the body weight of rats in the treatment group of the present invention began to increase after the second week of administration, indicating that the preparation of the present invention has no adverse effect on the body weight of rats.

[0042] The changes in forelimb and whole-body grip strength in rats are shown in Table 1, and the Lennon grade score and suspension time are shown in Table 2. As shown in Tables 1 and 2, compared with the model group, the Lennon scores of rats in each dosage group of the preparation of the present invention were significantly reduced, the forelimb and whole-body grip strength were significantly increased, the suspension time was significantly prolonged, and the serum AChR-Ab and calcium ion levels were significantly reduced (P<0.05 or P<0.01), suggesting that the preparation of the present invention can effectively improve the myasthenia gravis symptoms in EAMG rats.

[0043] Table 1. Data on changes in grip strength in the forelimbs and whole body of rats ( ±s)

[0044] Note: **P<0.01 compared with the control group; #P<0.05, ##P<0.01 compared with the model group; ΔP<0.05 compared with pre-treatment levels.

[0045] Table 2. Data on Lennon grade scores and suspension time in rats ( ±s)

[0046] Note: **P<0.01 compared with the control group; #P<0.05, ##P<0.01 compared with the model group.

[0047] Serum levels of AChR-ab and Ca in rats of each group after drug administration 2＋ Content detection results are shown below Figure 2 .like Figure 2 As shown, compared with the blank group, *P<0.05; **P<0.01; compared with the model group, #P<0.05, ##P<0.01.

[0048] 3.2 The repair effect of the formulation of this invention on pathological damage to the gastrocnemius muscle and brain tissue of EAMG rats like Figure 3 As shown, HE and Nissl staining results revealed that in the model group, the gastrocnemius muscle fibers of rats were atrophied and disorganized, and the neuronal nuclei in the brain tissue were pyknotted with a reduction in Nissl bodies. After intervention with the formulation of this invention, the gastrocnemius muscle fibers tended to be more regularly arranged, and the cross-sectional area per unit muscle fiber increased significantly; the morphology of neuronal cells in the brain tissue was restored, and the number of Nissl bodies increased, indicating that the formulation of this invention has a repairing effect on muscle and neuronal damage. It is evident that, compared with the model group, the gastrocnemius muscle fibers of rats in the formulation group of this invention were more regularly arranged and more morphologically intact.

[0049] like Figure 4 As shown, the cross-sectional area of ​​a single muscle fiber in rats treated with the formulation of this invention was significantly increased compared with that in the model group (P<0.01).

[0050] like Figure 5 As shown, the hippocampal neurons in the rats treated with the formulation of this invention showed significant recovery and more complete structure compared to the model group.

[0051] like Figure 6 As shown, the number of Nissl bodies in the rats treated with the formulation of this invention was reduced compared with that in the model group, and the Nissl body state was restored.

[0052] 3.3 The repair effect of the formulation of this invention on AChR at the neuromuscular junction in EAMG rats like Figure 7 As shown, immunofluorescence staining results revealed that the AChR morphology at the NMJ in the model group rats was incomplete, with both the area and number significantly reduced. After intervention with the formulation of this invention, AChR fragmentation was significantly improved, with both the area and number significantly increased (P<0.01), indicating that the formulation of this invention can repair the NMJ structure. It is evident that the red fluorescent patches of AChR at the NMJ of the gastrocnemius muscle in the rats treated with the formulation of this invention were more complete and larger in area than those in the model group.

[0053] like Figure 8 As shown, the morphology and number of AChRs at the NMJ in the hind paws of rats in the treatment group of the present invention were significantly improved compared with those in the model group.

[0054] like Figure 9As shown in the statistical analysis results, the area and quantity of AChR at the NMJ of rats in the administration group of the preparation of the present invention are both significantly increased compared with the model group (P<0.01).

[0055] 3.4 Effects of the preparation of the present invention on the expression of signaling pathway proteins in EAMG rats As shown in Figure 10 , the Western Blot results show that compared with the model group, the expression levels of AChR, PLC and MCOLN1 proteins in the brain tissue of rats in the administration group of the preparation of the present invention are all significantly increased (P<0.05 or P<0.01). Transcriptomic analysis further confirms that the differential gene MCOLN1 is up-regulated in the administration group and enriched in the calcium ion channel-related pathway. The results indicate that the therapeutic mechanism of the preparation of the present invention may be related to the activation of the AChR-PLC-MCOLN1-calcium signaling pathway. Figure 10 The Western Blot results and grayscale analysis show that the expression levels of AChR, PLC and MCOLN1 proteins in the administration group of the preparation of the present invention are all significantly higher than those in the model group.

[0056] As shown in Figure 11 , compared with the model group, a total of 160 differential genes are identified, of which 29 are up-regulated genes and 131 are down-regulated genes.

[0057] Example 7 Pharmacodynamic effect of the preparation of the present invention on urinary retention in rats with diabetic neurogenic bladder (DNB) 1. Experimental materials 1.1 Experimental animals: SPF-grade female SD rats, with a body weight of 220±10g. Purchased from the Animal Experiment Center of Xinjiang Medical University, the experimental animal production license number is SCXK (Xinjiang) 2019-0001. The animals are kept in the animal laboratory of Xinjiang Huashidan Pharmaceutical Research Co., Ltd., with a feeding environment of room temperature 22℃ to 27℃ and relative humidity of 40% to 60%. All operation steps in this experiment comply with the regulations of the National Science and Technology Commission on the administration of animal experimental research.

[0058] 1.2 Experimental drugs: the Uyghur medicinal composition preparation prepared in Example 1 of the present invention (hereinafter referred to as "the preparation of the present invention"), and the positive drug pyridostigmine bromide.

[0059] 2. Model establishment, intervention and index detection 2.1 Model establishment: A single intraperitoneal injection of streptozotocin (STZ, 65mg / kg) is performed to induce a diabetes model, and after continuous feeding for 12 weeks, a DNB urinary retention model is established.

[0060] 2.2 Grouping and Administration: Rats that successfully developed the model were randomly divided into a model group, a positive drug group (pyridostigmine bromide, 4.8 mg / kg), and low, medium, and high dose groups of the formulation of this invention (180, 360, and 720 mg / kg), with a normal control group. Each group consisted of 8 rats. The rats were administered the drug via gavage for 6 consecutive weeks, once daily.

[0061] 2.3 Detection indicators: fasting blood glucose, 2-hour and 12-hour urine output; results are shown in [link to results]. Figure 12 HE staining and LFB staining of bladder and brain tissue, results are shown in [link to results]. Figure 13-16 .

[0062] 3. Experimental Results 3.1 Effect of the formulation of the present invention on urine output in DNB rats like Figure 12 As shown, after 6 weeks of administration, compared with the model group, the 2-hour and 12-hour urine output of rats in each dose group of the preparation of the present invention was significantly increased (P<0.05 or P<0.01), and the effect was better than that of the positive control group, indicating that the preparation of the present invention can significantly improve the urination dysfunction of DNB rats. The results showed that compared with the model group, the 12-hour and 2-hour urine output of rats in the low, medium and high dose groups of the preparation of the present invention were significantly increased (P<0.01).

[0063] 3.2 The repair effect of the formulation of this invention on pathological damage to the bladder and brain tissue of DNB rats like Figure 13 As shown in the HE staining results, the model group rats exhibited significant hyperplasia of the bladder mucosal epithelium, smooth muscle hypertrophy, and disordered arrangement; the brain tissue also showed disordered neuronal arrangement and a reduced number of neurons. After intervention with the formulation of this invention, bladder epithelial hyperplasia was reduced, the muscle layer arrangement became more regular, and the morphology and density of neurons in the brain tissue were improved. LFB staining results showed severe demyelination of the brain tissue in the model group rats (lighter staining); after treatment with the formulation of this invention, the integrity of the myelin sheath was significantly restored (increased dark blue staining areas). This indicates that the formulation of this invention has a protective effect on central and peripheral nervous tissues.

[0064] like Figure 13 As shown, the pathological damage to the bladder tissue of rats in the treatment group of the present invention was significantly alleviated compared with that in the model group.

[0065] like Figure 14 As shown, the formulation of this invention significantly improved the recovery of neuronal cells in the brain tissue of rats.

[0066] like Figure 15 As shown, the depth and density of blue staining in the myelin sheath of rat brain tissue in the treatment group of the present invention were significantly restored compared with the model group.

[0067] like Figure 16As shown in the results of LFB staining of rat bladder tissue, compared with the model group, the staining depth and density of blue collagen fibers in the group treated with the preparation of this invention were significantly restored, the fiber arrangement tended to be more orderly, the disordered and sparse areas were reduced, and the structure was closer to the normal morphology.

[0068] Example 8 The protective effect of the formulation of this invention against LPS-induced inflammatory damage in PC12 cells. 1. Experimental Materials 1.1 Experimental Cells: Rat adrenal medullary pheochromocytoma cells (PC12 cells). Purchased from the cell bank of the Shanghai Branch of the Chinese Academy of Sciences, and cultured in the in vitro evaluation laboratory of Xinjiang Huashidan Pharmaceutical Research Co., Ltd. Culture environment: CO2 sterile incubator, 5% CO2 concentration, 37℃, 60-75% humidity.

[0069] 1.2 Experimental drug: The Uyghur medicine composition preparation prepared in Example 1 of the present invention (hereinafter referred to as "the preparation of the present invention").

[0070] 2. Model building, intervention and indicator detection 2.1 Model establishment: PC12 cells were stimulated with 1 μg / mL LPS to establish a neuroinflammatory cell model.

[0071] 2.2 Grouping and administration: A blank group, a model group (LPS), and low, medium, and high concentration groups of the formulation of this invention (31.25, 62.5, and 125 μg / mL) were set up.

[0072] 2.3 Detection indicators: MTT assay for cell viability; cell morphology observation and DAPI staining for apoptosis detection; Fluo-4AM fluorescent probe for intracellular Ca2+ detection. 2+ Concentration; TNF-α and IL-6 levels in cell supernatant were detected by ELISA. Results are shown below. Figure 17-20 .

[0073] 3. Experimental Results 3.1 Effect of the formulation of the present invention on the activity of PC12 cells MTT results showed that the formulation of the present invention had no significant effect on the proliferation rate of PC12 cells in the concentration range of 15.625~125 μg / mL, indicating that this concentration range is safe and non-toxic.

[0074] like Figure 17 As shown, compared with the blank group, the formulations of the present invention at all concentrations had no significant effect on the proliferation rate of PC12 cells (P>0.05).

[0075] 3.2 Effects of the formulation of this invention on LPS-induced PC12 cell morphology, apoptosis, and calcium levels. 2+ The influence of level Morphological observation and DAPI staining results showed that after LPS stimulation, PC12 cells became shrunken and rounded, and the number of apoptotic cells increased significantly. After intervention with the formulation of this invention, cell morphology gradually recovered, and apoptotic signals were significantly weakened. Fluo-4AM fluorescence staining results showed that intracellular Ca in the LPS group cells... 2+ The fluorescence intensity increased significantly. After administration of the formulation of this invention, intracellular Ca2+ levels increased. 2+ The levels decreased in a dose-dependent manner. This indicates that the formulation of the present invention can inhibit apoptosis and restore calcium homeostasis.

[0076] like Figure 18 As shown, the LPS group showed impaired cell morphology and increased apoptosis, while the formulation of the present invention showed improved cell morphology and reduced apoptosis in the treatment group.

[0077] like Figure 19 As shown, compared with the model group, the intracellular Ca2+ level in the drug-treated group of the present invention was significantly lower. 2+ The fluorescence intensity decreased significantly.

[0078] 3.3 Effects of the formulation of this invention on the expression of LPS-induced inflammatory factors in PC12 cells like Figure 20 As shown in the ELISA results, compared with the blank group, the levels of TNF-α and IL-6 in the cell supernatant of the LPS group were significantly increased. After intervention with the formulation of the present invention, the secretion levels of TNF-α and IL-6 were significantly decreased (P<0.01). This indicates that the formulation of the present invention can effectively inhibit the neuroinflammatory response. Compared with the model group, the levels of TNF-α and IL-6 in the cell supernatant of each concentration group of the formulation of the present invention were significantly reduced (P<0.01).

[0079] Example 9 Comparison of the efficacy of the Uyghur medicine composition preparations prepared in Example 1 and Comparative Example 2 against experimental autoimmune myasthenia gravis (EAMG) rats. Experimental groups: normal group, model group, positive drug group (prednisone tablets 5.4 mg / kg), low, medium and high dose groups of the drug composition in Example 1, and comparative example 1 drug composition.

[0080] Experimental method: Seventy female SD rats were acclimatized for one week, and 10 rats were randomly selected as the blank group. The remaining 60 rats were used for rat modeling. First, the mouse-derived AchR-α subunit 97-116 peptide sequence (R97-116), complete Freund's adjuvant (CFA), and phosphate buffered saline (PBS) were thoroughly mixed in a ratio of 1:2:2 to prepare an immunoemulsion (containing 50 μg per 200 μL).

[0081] First immunization: Except for the control group, all other groups of rats were injected subcutaneously with 200 μL of emulsion (containing 50 μg of R97-116) into the back and both hind paw pads. 50 μL of the emulsion was injected into each hind paw pad, and 100 μL of the immunoemulsion was injected subcutaneously into the back. The control group was injected subcutaneously with an equal volume of PBS.

[0082] Secondary immunization: On day 30 after the first immunization, the α-(97-116) peptide sequence, incomplete Freund's adjuvant (IFA), and PBS buffer were thoroughly mixed in a ratio of 1:2:2 to prepare a booster immunization emulsion. 200 μL of the prepared booster immunization emulsion (containing 50 μg of R97-116) was used for booster immunization, and the normal group was subcutaneously injected with an equal volume of PBS.

[0083] Final immunization: On day 45 after the first immunization, the α-(97-116) peptide sequence, incomplete Freund's adjuvant (IFA), and PBS buffer were thoroughly mixed in a ratio of 1:2:2 to prepare a booster immunization emulsion. 200 μL of the prepared booster immunization emulsion (containing 50 μg of R97-116) was used for the final booster immunization. The normal group was subcutaneously injected with an equal volume of PBS.

[0084] Test Results and Explanation (a) Model Evaluation: 1. Weight change: by Figure 21 It can be seen that the body weight of rats in both the model group and the blank group increased after the modeling began. The body weight of rats in the model group began to be lower than that of the normal group after day 27, and the statistical difference appeared on day 57 (P<0.05).

[0085] 2. Behavioral observation: The evaluator grasped the distal end of the rat's tail and hung it upside down. After the rat's forelimbs grasped the cage grid, the evaluator dragged it backward and upward until it resisted the evaluator and then released the grid. This was repeated for 30 seconds. All rats were evaluated according to the Lennon clinical symptom grading method. The scoring criteria are shown in Table 3 and the scoring results are shown in Table 4.

[0086] Table 3 Lennon Clinical Symptom Rating Table

[0087] Table 4. Clinical grade scores of rats in each group after drug administration ( ±s)

[0088] The average score of the model group is 1.13, which is greater than 1.

[0089] 3. Whole-body muscle strength measurement in rats: To avoid subjective bias in the assessment of Lennon's clinical symptoms, whole-body grip strength and forelimb grip strength were measured during the model assessment on day 60. The assessor lifted the rat by its tail, causing its forelimbs to grasp the grip plate, and gently pulled the rat backward parallel to the grip plate. The grip strength measuring instrument automatically read the maximum value (g). Results are shown below. Figure 22 .

[0090] Depend on Figure 22 It can be seen that the muscle strength of rats after modeling was significantly reduced compared with that of the control group (P<0.01).

[0091] 4. ELISA kit detection of antibody levels: Blood was collected from the tail vein one week after the last immunization. After standing for 30 minutes, the sample was centrifuged at 3000 rpm and 4°C for 15 minutes to extract serum. Serum AchR-Ab levels were detected using the ELISA method. The procedure was strictly performed according to the ELISA kit instructions. Serum AchR-Ab level results are shown below. Figure 23 .

[0092] Depend on Figure 23 It can be seen that AchR-ab was significantly increased in rats after modeling compared with the control group (P<0.01).

[0093] The establishment of the rat myasthenia gravis model was successfully assessed based on model evaluation indicators such as rat body weight change, muscle strength, Lennnon score, and antibody content. Among 62 rats, 45 rats developed myasthenia gravis, and the model success rate was 45 / 62 × 100% = 72.58%.

[0094] (II) Effects of the Examples on Myasthenia Symptoms in EAMG Rats 1. Rat body weight curve From the first dose, evaluators (not the injection personnel) measured rat weight every 2 days. After the modeling period, the data were plotted as a rat weight change curve. Figure 24 .

[0095] Depend on Figure 24 It is evident that the body weight of the rat model group continued to decrease, while the body weight of rats in each drug administration group increased.

[0096] 2. Cage Turning Test As required by the literature, a cage-turning test was performed after the last immunization to quantitatively assess muscle weakness. The cage-turning test method was as follows: the rat was placed in the center of a wire mesh screen, immediately rotated to an inverted position, and stably held 50 cm above the pad surface. The time it took for the rat to fall off the pad was measured, with the endpoint being 300 seconds. Results are shown below. Figure 25 .

[0097] Depend on Figure 25As can be seen, compared with the blank group, the suspension time of rats in the model group was significantly reduced. After administration, compared with the model group, the suspension time of rats in the positive group was significantly increased. The difference was statistically significant (P < 0.05). The suspension time of rats in the low, medium and high dose groups of Epimeline and the original prescription dose group was significantly increased, and the difference was statistically significant (P < 0.01).

[0098] 3. Changes in grip strength Changes in grip strength in rats of each group after drug administration are shown in the figure. Figure 26 .

[0099] Depend on Figure 26 As can be seen, compared with the blank group, the muscle strength of the rats in the model group was significantly reduced, and the difference was statistically significant (P<0.01). After administration, compared with the model group, the muscle strength of the rats in the positive group and the rats in the low / medium dose group of ibemantin was significantly increased, and the difference was statistically significant (P<0.05). Compared with the model group, the muscle strength of the original prescription dose group was significantly increased, and the difference was statistically significant (P<0.01). Compared with the rats in the model group, there was no statistically significant difference in muscle strength of the rats in the high dose group of ibemantin (P>0.05).

[0100] 4. Effects on AchR-ab levels in EAMG rats Effects of drug administration on AchR-ab levels in EAMG rats are shown in the following figures. Figure 27 .

[0101] Depend on Figure 27 As can be seen, compared with the blank group, the AchR-ab content in the model group rats was significantly increased (P < 0.01), and the difference was statistically significant. Compared with the model group, the AchR-ab content in the positive drug group, the low / high dose group of Abimantin, and the original prescription dose group was significantly decreased (P < 0.01), and the difference was statistically significant. The AchR-ab content in the medium dose group of Abimantin was significantly decreased (P < 0.05), and the difference was statistically significant.

[0102] 5. Sections of rat brain and gastrocnemius muscle tissue Rat brain tissue sections Figure 28 Sections of rat gastrocnemius muscle tissue are shown Figure 29 Nissl staining of brain tissue sections Figure 30 .

[0103] Depend on Figure 28As can be seen, HE staining revealed that the cell nuclei were purplish-blue and the cytoplasm was red. The normal group showed clear brain tissue structure, regular cell arrangement, and no obvious pathological changes such as edema, inflammatory cell infiltration, tissue proliferation, or damage, representing healthy brain tissue morphology. In the model group, the perivascular spaces were widened, the tissue was loose, edema was observed, and the cell arrangement was disordered, indicating possible brain tissue damage. The pathological changes in the positive drug group were significantly reduced compared to the model group: perivascular abnormalities were improved, and the tissue morphology was closer to that of the normal group. The pathological changes in the low-dose group were slightly alleviated compared to the model group, but some degree of tissue abnormality still existed. The pathological improvement in the medium-dose group was more significant, approaching the effect of the positive drug group. In the high-dose group, the tissue morphology was further restored, with less difference from the normal group, indicating that the drug had a more prominent effect on improving brain tissue damage at high doses.

[0104] Depend on Figure 29 As observed by HE staining, the normal group showed tightly and neatly arranged muscle fibers, narrow and uniform intermuscular spaces, regular muscle fiber morphology, and uniform staining, with no inflammatory cell infiltration or structural damage. The model group exhibited significant pathological changes: disordered and loose muscle fiber arrangement, with some muscle fibers possibly showing breakage / degeneration; significantly widened intermuscular spaces, suggesting muscle tissue edema, interstitial hyperplasia, or inflammatory response. Positive drug group: The intermuscular space was smaller than that of the model group, and the arrangement of muscle fibers was closer to that of the normal group, suggesting that the drug can improve pathological damage; In each drug group: the intermuscular spaces narrowed and the muscle fiber arrangement became more regular in the medium-dose group, suggesting that the medium-dose group may have better efficacy.

[0105] Depend on Figure 30 As can be seen, Nissl staining showed that Nissl bodies (dark blue granular structures, mainly distributed in neuronal cell bodies and dendrites) were evenly distributed and of moderate density in the normal group, with neurons arranged in a regular manner. In the model group, Nissl bodies stained darker and had a significantly increased density (the dark blue area was more concentrated and thicker); the neuronal arrangement was disordered, suggesting that the brain tissue may have experienced inflammatory responses, neuronal stress, or damage, leading to compensatory proliferation or aggregation of Nissl bodies. In the positive drug group, the density and staining intensity of Nissl bodies were significantly reduced, more closely resembling the uniform distribution of the normal group, indicating that the positive drug can improve Nissl body abnormalities under pathological conditions. In the low-dose group, Nissl bodies still showed some degree of dense staining, but this was less than in the model group, indicating limited repair effect. In the medium-dose group, the density of Nissl bodies was further reduced, and the staining was more uniform, showing a better repair effect than the low-dose group. In the high-dose group, the distribution and density of Nissl bodies were close to the normal group, suggesting that the higher the drug dose, the more significant the improvement effect on Nissl body abnormalities, exhibiting a dose-dependent repair effect.

[0106] The Uyghur medicine composition provided by this invention, through in vitro and in vivo experiments, has been shown to effectively improve myasthenia gravis symptoms in EAMG rats, increase urine output in DNB rats, repair neuromuscular junction structures, protect neuronal and myelin sheath integrity, and inhibit neuroinflammatory responses. Its mechanism of action is closely related to the regulation of the AChR-PLC-MCOLN1 signaling pathway and the downregulation of inflammatory factors such as TNF-α and IL-6. This formulation has the advantages of multi-target and multi-pathway therapy, with few toxic side effects, providing new drug options and experimental evidence for the treatment of neuromuscular junction diseases, and has significant clinical translational value and broad application prospects.

[0107] 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. A Uyghur medicine composition for treating neuromuscular junction diseases, characterized in that, The preparation comprises the following raw materials in parts by weight: 5-30 parts of camel bud, 5-30 parts of aloe vera, 5-30 parts of asafoetida, 5-30 parts of myrrh, 5-30 parts of patchouli, 5-30 parts of mustard seed, 5-30 parts of twig root, and 5-100 parts of chebula.

2. The Uyghur medicine composition formulation as described in claim 1, characterized in that, The preparation contains the following raw materials in parts by weight: 20 parts of camel bud, 20 parts of aloe vera, 20 parts of asafoetida, 20 parts of myrrh, 20 parts of patchouli, 20 parts of mustard seed, 20 parts of twig root, and 100 parts of chebula.

3. The Uyghur medicine composition formulation as described in claim 1, characterized in that, The Uyghur medicine composition also includes a pharmaceutically acceptable carrier; the dosage form is capsule, tablet, granule, pill or powder.

4. A method for preparing a Uyghur medicine composition for treating neuromuscular junction diseases, characterized in that, Includes the following steps: (1) Weigh out the processed camel buds, patchouli, mustard seeds, box fruit vine roots, and Terminalia chebula according to the weight proportions; (2) Add water to the medicinal materials obtained in step (1) to extract, filter, and obtain the extract; (3) Concentrate the extract obtained in step (2) and dry it to obtain the extract powder; (4) The extract powder obtained in step (3) is mixed with asafoetida, aloe vera, myrrh and pharmaceutically acceptable excipients to prepare a Uyghur medicine composition preparation.

5. The preparation method according to claim 4, characterized in that, The extraction described in step (2) is a decoction extraction, which is performed 2 to 3 times, with each extraction lasting 1 to 3 hours, and the amount of water added each time being 8 to 15 times the total weight of the medicinal materials.

6. The preparation method according to claim 4, characterized in that, The concentration in step (3) is vacuum concentration, with a temperature of 50~70℃ and a vacuum degree of -0.075~-0.095MPa; the drying is spray drying or vacuum drying, and the moisture content of the dried powder is ≤5.0%.

7. The preparation method according to claim 4, characterized in that, The pharmaceutically acceptable excipients mentioned in step (4) are selected from one or more of fillers, binders, flow aids, and lubricants.

8. A capsule formulation of a Uyghur medicine composition prepared using the preparation method according to claim 4, characterized in that, The weight ratio of the extract powder to microcrystalline cellulose, microcrystalline silica gel and magnesium stearate is 85:12:2:

1.

9. The use of the Uyghur medicine composition formulation as described in any one of claims 1-3 in the preparation of a medicament for the prevention and / or treatment of neuromuscular junction diseases.

10. The application as described in claim 9, characterized in that, The neuromuscular junction diseases include myasthenia gravis or neurogenic bladder.

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