Application of ganoderma applanatum active component in preparation of medicine for treating myocardial ischemia

Abstract

The invention relates to the technical field of medicines, and discloses application of ganoderma lipsiense active ingredients in preparation of medicines for treating myocardial ischemia. Through a rat chronic myocardial ischemia injury model, it is proved that the ganoderma lipsiense active component can relieve myocardial ischemia, protect myocardial contraction and relaxation functions, reduce persistent necrosis of myocardial cells, reduce myocardial cell injury and relieve myocardial ischemia in the aspects of echocardiogram, hemodynamics, myocardial infarction area, heart visceral index, serum biochemical index and the like. The chronic myocardial ischemia process is inhibited. Research results show that the ganoderma lipsiense active component can be used as a pharmaceutical active component for treating myocardial infarction diseases caused by myocardial necrosis and the like caused by myocardial ischemia.

Description

Technical Field

[0001] The invention relates to the technical field of medicines, and in particular to the application of active ingredients of Ganoderma lucidum in preparing medicines for treating myocardial ischemia. Background Art

[0002] Myocardial ischemia is the main cause of morbidity and mortality in cardiovascular disease patients worldwide. On the basis of coronary artery lesions, the blood flow of the coronary arteries is sharply reduced or interrupted, causing severe and persistent ischemia of the corresponding myocardium, which eventually leads to myocardial necrosis and myocardial infarction (MI). The incidence and mortality of myocardial infarction (MI) in my country have been increasing year by year. Therefore, how to treat myocardial ischemia has always been a concern of the world.

[0003] Ganoderma applanatum (Pers.) Pat. is a large basidiomycete belonging to Amastigomycota, Basidiomycota, Aphyllophorales, Polyporaceae, and Ganoderma. As a kind of edible fungus, it contains a variety of chemical components, such as polysaccharides, amino acids, alkaloids, triterpenes, flavonoids, steroidal compounds, unsaturated fatty acids, and trace elements such as zinc and iron. According to literature records, Ganoderma applanatum has the effects of anti-tumor, anti-virus, antibacterial and anti-inflammatory, bidirectional blood pressure regulation, blood sugar reduction, arteriosclerosis prevention, analgesia, anti-oxidation, and immunity enhancement. At present, there is no report on the active ingredients of Ganoderma applanatum for treating myocardial ischemia-related diseases. Therefore, the present invention establishes a rat chronic MI model to study the effect of the active ingredients of Ganoderma applanatum on treating MI, so as to provide a reference for clinical search for better drugs for treating myocardial ischemia. Summary of the invention

[0004] The purpose of the present invention is to provide an application of an active ingredient of Ganoderma lucidum in the preparation of a drug for treating myocardial ischemia, which can be used to prepare a drug for treating myocardial infarction caused by myocardial necrosis due to myocardial ischemia.

[0005] In order to achieve the above object, the technical solution of the present invention is as follows:

[0006] The invention discloses an application of an active ingredient of Ganoderma lucidum in preparing a drug for treating myocardial ischemia. The active ingredient of Ganoderma lucidum is triterpenoids of Ganoderma lucidum or a combination of triterpenoids of Ganoderma lucidum and polysaccharides of Ganoderma lucidum.

[0007] Furthermore, the purity of the triterpenes of Ganoderma lucidum is not less than 80%, and the purity of the polysaccharide of Ganoderma lucidum is not less than 75%.

[0008] Furthermore, the mass concentration ratio of Ganoderma lucidum triterpenoids to Ganoderma lucidum polysaccharide in the combination of Ganoderma lucidum triterpenoids and Ganoderma lucidum polysaccharide is 3:2.

[0009] Furthermore, the active ingredients of Ganoderma lucidum relieve myocardial ischemia damage by protecting myocardial contraction and relaxation functions.

[0010] Furthermore, the active ingredients of Ganoderma lucidum relieve myocardial ischemic damage by reducing the sustained necrosis of myocardial cells.

[0011] Furthermore, the active ingredients of Ganoderma lucidum relieve myocardial ischemic damage by reducing inflammatory edema of myocardial tissue and lowering inflammatory response.

[0012] Furthermore, the active ingredients of Ganoderma lucidum inhibit the progression of heart failure by reducing myocardial cell damage.

[0013] Furthermore, the drug also contains pharmaceutically acceptable excipients.

[0014] Furthermore, the pharmaceutically acceptable excipient is one or more of a diluent, an excipient, a filler, a binder, a wetting agent, a disintegrant, an absorption promoter, a surfactant, an adsorption carrier and a lubricant.

[0015] Furthermore, the medicine is an oral preparation or an injection.

[0016] In summary, the present invention has the following beneficial effects:

[0017] According to the characteristics of myocardial ischemic heart disease, the present invention prepares a rat chronic myocardial ischemic injury model by ligating LAD for 4 weeks, and conducts experiments such as echocardiography, hemodynamics, myocardial infarction area, cardiac organ index and serum biochemical indexes. The experimental results show that the active ingredients of Ganoderma lucidum (Ganoderma lucidum triterpenes and Ganoderma lucidum triterpenes and Ganoderma lucidum polysaccharide combination) can relieve myocardial ischemia, protect myocardial contraction and relaxation functions, reduce persistent myocardial cell necrosis, reduce inflammatory edema of myocardial tissue, reduce inflammatory response, reduce myocardial cell damage, and inhibit the progression of heart failure. The research results of the present invention show that the active ingredients of Ganoderma lucidum can be used as a pharmaceutical active ingredient to treat myocardial infarction diseases caused by myocardial ischemia and myocardial necrosis. BRIEF DESCRIPTION OF THE DRAWINGS

[0018] Figure 1The effects of the active ingredients of Ganoderma lucidum on various echocardiographic indices of MI rats (A is the effect on the left ventricular ejection fraction EF, a cardiac function index; B is the effect on the left ventricular short axis shortening rate FS, a cardiac function index; C is the effect on the diastolic interventricular septum IVSd, a cardiac structure index; D is the effect on the end-systolic thickness IVSs, a cardiac structure index; E is the effect on the diastolic left ventricular posterior wall LVPWd, a cardiac structure index; F is the effect on the end-systolic thickness LVPWs, a cardiac structure index; n=6, compared with the sham operation group; *** P < 0.001, * P<0.05; compared with the model group, # P<0.05, ## 0.001<P<0.01);

[0019] Figure 2 The effects of the active ingredients of Ganoderma lucidum on the hemodynamics of MI rats (A is the effect on the left ventricular systolic pressure LVSP, B is the effect on the left ventricular end-diastolic pressure LVEDP, C is the maximum rate of change of left ventricular pressure +dp / dt max The influence of left ventricular pressure, D is the minimum rate of change of left ventricular pressure - dp / dt mix n = 6, compared with the sham operation group, ** 0.001<P<0.01, *** P<0.001; compared with the model group, # P<0.05, ## 0.001<P<0.01);

[0020] Figure 3 This is a representative picture of the effect of the active ingredients of Ganoderma lucidum on the myocardial infarction area of ​​MI rats in the present invention (n=6);

[0021] Figure 4 The effects of the active ingredients of Ganoderma lucidum on myocardial infarction area and biochemical indexes in MI rats (A is the effect on myocardial infarction area, B is the effect on cardiac organ index, C is the effect on biochemical index cTnI, D is the effect on biochemical index BNP, E is the effect on biochemical index sST2, and F is the effect on biochemical index Galectin-3; n=6, compared with the sham operation group, * P<0.05, ** 0.001<P<0.01, *** P<0.001; compared with the model group, # P<0.05). DETAILED DESCRIPTION

[0022] In order to enable those skilled in the art to better understand the solution of the present invention, the technical solution of the present invention will be further described in detail below in conjunction with the embodiments of the present invention and the accompanying drawings. Obviously, the described embodiments are only part of the embodiments of the present invention, not all of the embodiments. Based on the embodiments of the present invention, all other embodiments obtained by ordinary technicians in this field without creative work should fall within the scope of protection of the present invention.

[0023] It should be noted that, in the absence of conflict, the embodiments and features of the embodiments of the present invention can be combined with each other. The present invention will be described in detail below in conjunction with the embodiments.

[0024] Example:

[0025] 1 Experimental Materials

[0026] 1.1 Experimental animals

[0027] Healthy adult SD rats, SPF grade, male, weighing 200±20 g, were provided by Jinhua Research Institute of Zhejiang Chinese Medical University, animal license number: SYXK(Zhejiang)2024-0027, certificate number: 20240004025638.

[0028] 1.2 Drugs and reagents

[0029] Ganoderma lucidum polysaccharide (self-made in the laboratory, batch number 20240318, purity 78.1%, brown powder); Ganoderma lucidum triterpenoids (self-made in the laboratory, batch number 20240321, purity 82%, dark brown powder); Metoprolol succinate sustained-release tablets (batch number 20231201, AstraZeneca Pharmaceuticals Co., Ltd.); Amoxicillin tablets (batch number 013231181, Shijiazhuang Pharmaceutical Group Zhongnuo Pharmaceutical Co., Ltd.); Sodium carboxymethyl cellulose (batch number 20231212, Shanghai Zhanyun Chemical Co., Ltd.); 10% chloral hydrate (batch number 20240314, Shandong Puhuifen Chemical Technology Co., Ltd.); cTnI (cardiac troponin I), BNP (brain natriuretic peptide), sST2 (soluble growth stimulation expression gene 2 protein), Galectin-3 (galactose lectin 3) test kits were all purchased from Nanjing Jiancheng Bioengineering Institute, batch number 20240519.

[0030] The positive control drug metoprolol and the tested drugs Ganoderma lucidum polysaccharide and Ganoderma lucidum triterpenoid were all administered by oral gavage using a suspension prepared with 0.5% sodium carboxymethyl cellulose. The drugs were prepared on the same day and used immediately after preparation.

[0031] 1.3 Main instruments and equipment

[0032] Small animal ventilator (model: ALC-V8S, Shanghai ALCOT Biotechnology Co., Ltd.); multi-channel biological signal analysis system (model: ALC-MPA, Shanghai ALCOT Biotechnology Co., Ltd.); echocardiograph (model: ACUSONJuniper S, Shanghai Siemens Medical Devices Co., Ltd.); electronic balance (model: AR1140, Mettler-Toledo Instrument Co., Ltd.); point mixer (model LC-Vortox-P2, Shanghai Lichen Bangxi Instrument Technology Co., Ltd.); microplate reader (model: M200 Pro Nanoquant, Shanghai Diken Trading Co., Ltd.); refrigerated centrifuge (model: AuegraX30R, Beckman Company).

[0033] 2 Experimental methods

[0034] 2.1 Animal grouping and treatment

[0035] After purchase, SD male rats were raised in an SPF environment with room temperature of 23℃~26℃ and relative humidity of 40%~60% for 3 days with free access to food and water. After 3 days, SD rats with a body weight of 300±30g were selected and randomly divided into 6 groups. That is, sham operation model group (Sham), chronic myocardial ischemia model group (M), metoprolol succinate group (MT), Ganoderma lucidum polysaccharide group (GLP), Ganoderma lucidum triterpenoid group (GLT), Ganoderma lucidum polysaccharide + Ganoderma lucidum triterpenoid combination group (GLP+GLT), with 6 rats in each group. Rats were raised in an SPF environment with free access to food and water.

[0036] 2.2 Preparation of experimental model

[0037] 2.2.1 Preoperative preparation

[0038] The rats were weighed and anesthetized with 10% chloral hydrate solution by intraperitoneal injection. The rats' reactions were observed. After the corneal reflex and muscle tension disappeared, the rats were placed on a mouse board and fixed in a supine position with a rope. The rats were disinfected with iodine and their skin was prepared. The respiratory rate of the small animal ventilator was adjusted to 90 times / min and the tidal volume to 2.0 mL / time. The rats' necks were opened and connected to the small animal ventilator.

[0039] 2.2.2 MI model preparation surgery

[0040] After connecting the ventilator and observing for 2 minutes, the rats were breathed steadily. The thoracotomy was performed layer by layer at the 3rd to 4th ribs in the left chest, the pericardium was separated, the heart was exposed, and the LAD was ligated 2 mm below the left atrial appendage with a suture needle. The myocardium below the ligation point turned pale or regional myocardial dyskinesia occurred, which was a sign of successful ligation. After ligation, the heart was returned to the chest cavity, the heart and lungs were adjusted to normal position, and the wound was sutured layer by layer. The sham operation model group rats underwent the same surgical procedure as the MI model rats, but only a silk thread was left under the left coronary artery, and no ligation was performed.

[0041] 2.2.3 Postoperative recovery

[0042] After the operation, amoxicillin powder was sprinkled on the wounds on the chest and neck of the rats, and the rats were gently removed from the mouse board and placed on a pet electric blanket to keep warm until the anesthetic effect subsided and consciousness recovered.

[0043] 2.3 Administration

[0044] Each group of rats was given continuous oral administration for 28 days, once a day, and the amount of each oral administration was calculated based on the body weight of the day. The MI and Sham groups were given 0.5% sodium carboxymethylcellulose solution, the MT group was given metoprolol succinate solution, the GLP group was given 0.01% Ganoderma lucidum polysaccharide solution, the GLT group was given 0.015% Ganoderma lucidum triterpenoid solution, and the GLP+GLT combination group was given 0.01% Ganoderma lucidum polysaccharide and 0.015% Ganoderma lucidum triterpenoid solution.

[0045] 2.4 Index detection

[0046] 2.4.1 Doppler echocardiography

[0047] After anesthesia, the rats were shaved of their left chest hair, and a small amount of coupling agent was applied before echocardiography. The data from echocardiography were averaged using three consecutive tests. The monitoring indicators included: (1) cardiac function indicators: left ventricular ejection fraction (EF) and left ventricular fractional shortening (FS); (2) cardiac structure indicators: interventricular septum diastolic / end-systolic thickness (IVSd / IVSs) and left ventricular posterior wall diastolic / end-systolic thickness (LVPWd / LVPWs).

[0048] 2.4.2 Hemodynamics

[0049] After the echocardiogram, the changes of left ventricular hemodynamics were monitored and the cardiac systolic and diastolic functions were evaluated. The observation indexes included left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), the maximum rate of pressure rise and fall (+dp / dt max ) and the minimum rate of change of left ventricular pressure (the miximum rate ofpressure rise and fall, -dp / dt mix ).

[0050] 2.4.3 Myocardial infarction area

[0051] After the heart was weighed, it was cut into 5 slices from the apex to the root of the heart. Each myocardial slice was fixed with 4% paraformaldehyde tissue fixative for 24 hours, dehydrated, embedded in paraffin, cut into 5 μm slices, and stained with Masson (this part of the experiment was commissioned by Nanjing Youmeng Biotechnology Co., Ltd.). The percentage of myocardial infarction area was determined using computer image analysis software Image Pro Plus.

[0052] Myocardial infarction area percentage = (myocardial infarction blue-stained area area / (myocardial infarction blue-stained area area + normal myocardium red-stained area area) × 100%.

[0053] 2.4.4 Heart organ index

[0054] Heart organ coefficient = (heart weight / body weight) × 100%, body weight is the body weight at the last administration.

[0055] 2.4.5 Determination of serum cTnI, BNP, sST2, and Galectin-3 levels

[0056] After the hemodynamics was determined, 4 mL of blood was collected from the rat carotid artery, kept at 4°C for 1 h, centrifuged at 3500 r / min for 10 min, and the serum was divided into EP tubes and stored at -80°C. The contents of cTnI, BNP, sST2, and Galectin-3 in serum were detected strictly according to the instructions of the kit.

[0057] 2.5 Statistical analysis

[0058] All data were analyzed using SPSS 13.0 software. The t-test was used for comparison between the two groups, and one-way analysis of variance was used for comparison within multiple groups. The experimental results are presented as mean ± standard deviation. express.

[0059] 3 Experimental results

[0060] 3.1 Effects of active ingredients from Ganoderma lucidum on echocardiographic cardiac function and cardiac structure in rats with chronic myocardial ischemia

[0061] The cardiac function and cardiac structure of MI rats were changed. Compared with the sham group, the LVPWd of the cardiac structure of the MI model group rats increased significantly (P < 0.001), and IVSd, IVSs and LVPWs decreased significantly (P < 0.01 or P < 0.001). Myocardial ischemia also occurred in the posterior wall of some MI rats. At the same time, EF and FS of MI rats decreased significantly (P < 0.001). After 4 weeks of continuous treatment with the active ingredients of Ganoderma lucidum, the cardiac function indexes EF and FS of the rats in the Ganoderma lucidum triterpenoid group and Ganoderma lucidum polysaccharide + triterpenoid group were significantly increased compared with the MI model group (P < 0.05 or 0.001 < P < 0.01). At the same time, the cardiac structure indexes were also alleviated, as shown by the significant increase of IVSd, IVSs and LVPWs (P < 0.05 or 0.001 < P < 0.01), and the increase of LVPWd (P < 0.05).

[0062] 3.2 Effects of active ingredients from Ganoderma lucidum on hemodynamics in rats with chronic myocardial ischemia

[0063] Analysis of hemodynamic indicators showed that the cardiac function of MI rats changed significantly, as shown by LVSP and +dp / dt max The LVEDP and -dp / dt max The significant increase (0.001<P<0.01 or P<0.001) indicated that the cardiac diastolic and contractile abilities of the rats in the model group were damaged. After 4 weeks of continuous treatment with the active ingredients of Ganoderma lucidum, the LVSP and +dp / dt of the rats in the Ganoderma lucidum triterpenoid group and the Ganoderma lucidum polysaccharide + triterpenoid group were significantly increased. max Significantly increased (P<0.05 or 0.001<P<0.01), LVEDP and -dp / dt max The results showed that the cardiac contraction and relaxation abilities of rats were restored after the synergistic treatment with the active ingredients of Ganoderma lucidum.

[0064] 3.3 Effects of active ingredients from Ganoderma lucidum on myocardial infarction area in rats with chronic myocardial ischemia

[0065] Cardiac morphological changes and myocardial infarction area are the most intuitive indicators for evaluating the disease status of MI rats. Figure 3As shown in the figure, 4 weeks after LAD ligation, gray-white scar tissue formed on the surface of the rat heart, the left ventricular anterior wall myocardium became thinner, obvious myocardial ischemia area appeared, and the left ventricle dilated and hypertrophied to varying degrees. After Masson staining of myocardial sections, the infarct area was replaced by blue collagen fibers (scar tissue), and the area of ​​myocardial infarction increased significantly (P < 0.001). Figure 4 -A, compared with the model group, the myocardial infarction area of ​​rats in the Ganoderma lucidum triterpenoid group and the Ganoderma lucidum triterpenoid combined with Ganoderma lucidum polysaccharide group was significantly reduced (P < 0.05), showing an ideal therapeutic effect.

[0066] 3.4 Effects of active ingredients from Ganoderma lucidum on cardiac organ indexes in rats with chronic myocardial ischemia

[0067] like Figure 4 -B, the cardiac organ index of the rats in the model group was significantly higher than that in the sham operation group (P<0.05). Compared with the model group, the cardiac organ index of the rats treated with Ganoderma lucidum triterpenoids group and Ganoderma lucidum triterpenoids combined with polysaccharides group returned to normal trend (P<0.05).

[0068] 3.5 Effects of active ingredients from Ganoderma lucidum on biochemical parameters in rats with chronic myocardial ischemia

[0069] Serum biochemical indicators are common indicators of MI pathology. Serum cTnI was detected to detect myocardial injury in rats, and BNP, sST2 and Galectin-3 were selected to evaluate the degree of heart failure in MI rats. Figure 4 As shown in CF, compared with the sham operation group, the levels of cTnI, BNP, sST2 and Galectin-3 in the serum of the model group rats were significantly higher than those in the sham operation group (P<0.05 or 0.001<P<0.01 or P<0.001), and significant myocardial damage and heart failure occurred. Compared with the model group, after 4 weeks of treatment with the active ingredients of Ganoderma lucidum, the serum cTnI content of MI rats decreased (P<0.05), and the levels of BNP, sST2 and Galectin-3 (P<0.05) were inhibited to a certain extent, among which the triterpenoid group of Ganoderma lucidum combined with polysaccharide group had the most obvious effect in inhibiting heart failure.

[0070] Clinically, persistent ischemia and hypoxia in the coronary arteries cause myocardial necrosis, trigger a persistent inflammatory response, and gradually cause myocardial cell apoptosis, decreased myocardial contractility, and fibrosis of some myocardial cells, which lose their systolic and diastolic functions. The surviving myocardial tissue still suffers from ischemia and hypoxia, and the cardiac output is insufficient and the reflux is impaired, leading to gradual left ventricular hypertrophy and concurrent dysfunction of various organ systems, leading to ventricular remodeling. Chronic myocardial ischemia can eventually develop into heart failure. As the terminal stage of various heart diseases, ischemic heart failure progresses rapidly, with poor treatment effects and difficult to control conditions. The hospitalization rate, morbidity and mortality rates of patients are generally high, threatening the health and life of patients.

[0071] The degree of myocardial ischemia is closely related to left ventricular function, echocardiographic indexes EF, FS and hemodynamic indexes LVSP, LVEDP, ±dP / dt max It is an important indicator reflecting the systolic and diastolic function of the heart. As the degree of myocardial ischemia deepens, the structure of the heart will also change, which is reflected in the changes of IVSs, IVSd, IVSs and LVPWs. The quantitative histological method for determining the area of ​​myocardial infarction is the most intuitive evaluation indicator for myocardial ischemia research. CTnI is a marker of myocardial damage. When myocardial cells are damaged and the integrity of the cell membrane is destroyed, myocardial enzymes will leak out and be released into the blood. This is often used to diagnose the degree of myocardial damage in clinical practice. Serum BNP, sST2 and Galectin-3 levels reflect whether heart failure occurs after myocardial damage. The present invention is intended to carry out anti-MI pharmacodynamics research on the main active ingredients of Ganoderma lucidum, so as to provide a reference for the clinical search for better myocardial protective drugs.

[0072] According to the characteristics of myocardial ischemic heart disease, the present invention prepares a rat chronic myocardial ischemic injury model by ligating LAD for 4 weeks, selects the clinical first-line treatment drug β-receptor blocker metoprolol as the positive control drug for animal experiments, and explores the myocardial protective effect of the active ingredients of Ganoderma lucidum from the aspects of echocardiography, hemodynamics, myocardial infarction area, cardiac organ index, serum biochemical indexes, etc. The results show that compared with the MI model group, the Ganoderma lucidum triterpene group and the triterpene combined with polysaccharide treatment group rats: ① The echocardiographic indexes improved, as shown by a significant increase in EF, FS, IVSd, IVSs and LVPWs, and a decrease in LVPWd, indicating that the Ganoderma lucidum triterpene group and the triterpene combined with polysaccharide group intervention can alleviate myocardial ischemia; ② The hemodynamic indexes were significantly improved, as shown by LVSP and +dP / dt max Rise, LVEDP and -dP / dt max③ The myocardial infarction area decreased significantly, indicating that the triterpenoids of Ganoderma lucidum and the triterpenoids combined with polysaccharides pretreatment had a protective effect on the left ventricular systolic and diastolic function of MI rats; ④ The cardiac organ index decreased, indicating that the triterpenoids of Ganoderma lucidum and the triterpenoids combined with polysaccharides could reduce the persistent necrosis of myocardial cells; ⑤ The CTnI level reflecting the degree of myocardial damage was decreased, indicating that the active ingredients of Ganoderma lucidum could reduce myocardial cell damage. The results of other biochemical indicators showed that the process of heart failure in rats was inhibited after treatment with the active ingredients of Ganoderma lucidum.

[0073] In summary, the triterpenes from Ganoderma lucidum and the triterpenes combined with polysaccharides from Ganoderma lucidum of the present invention have obvious protective effects on chronic myocardial ischemia injury.

[0074] The above-described embodiments only express the preferred implementation modes of the present invention, and the descriptions thereof are relatively specific and detailed, but they cannot be understood as limiting the scope of the present invention. It should be pointed out that, for those of ordinary skill in the art, several modifications and improvements can be made without departing from the concept of the present invention, and these all belong to the protection scope of the present invention. Therefore, the protection scope of the present invention shall be subject to the attached claims.

Claims

1. The use of active ingredients of Ganoderma lucidum in the preparation of a drug for treating myocardial ischemia, characterized in that: The active ingredient of Ganoderma lucidum is Ganoderma lucidum triterpenoid or a combination of Ganoderma lucidum triterpenoid and Ganoderma lucidum polysaccharide.

2. The use of the active ingredient of Ganoderma lucidum according to claim 1 in the preparation of a drug for treating myocardial ischemia, characterized in that: The purity of the triterpenoids of Ganoderma lucidum is not less than 80%, and the purity of the polysaccharide of Ganoderma lucidum is not less than 75%.

3. The use of the active ingredient of Ganoderma lucidum according to claim 1 in preparing a drug for treating myocardial ischemia, characterized in that: The mass concentration ratio of Ganoderma lucidum triterpenoids to Ganoderma lucidum polysaccharide in the combination of Ganoderma lucidum triterpenoids and Ganoderma lucidum polysaccharide is 3:

2.

4. The use of the active ingredient of Ganoderma lucidum according to claim 1 in preparing a drug for treating myocardial ischemia, characterized in that: The active ingredients of Ganoderma lucidum relieve myocardial ischemia damage by protecting myocardial contraction and relaxation functions.

5. The use of the active ingredient of Ganoderma lucidum according to claim 1 in preparing a drug for treating myocardial ischemia, characterized in that: The active ingredients of Ganoderma lucidum relieve myocardial ischemia damage by reducing persistent necrosis of myocardial cells.

6. The use of the active ingredient of Ganoderma lucidum according to claim 1 in preparing a drug for treating myocardial ischemia, characterized in that: The active ingredients of Ganoderma lucidum relieve myocardial ischemic damage by reducing inflammatory edema of myocardial tissue and lowering inflammatory response.

7. The use of the active ingredient of Ganoderma lucidum according to claim 1 in preparing a drug for treating myocardial ischemia, characterized in that: The active ingredients of Ganoderma lucidum inhibit the progression of heart failure by reducing myocardial cell damage.

8. The use of the active ingredient of Ganoderma lucidum in the preparation of a drug for treating myocardial ischemia according to claim 1, characterized in that: The medicine also contains pharmaceutically acceptable excipients.

9. The use of the active ingredient of Ganoderma lucidum according to claim 1 in preparing a drug for treating myocardial ischemia, characterized in that: The pharmaceutically acceptable auxiliary material is one or more of a diluent, an excipient, a filler, a binder, a wetting agent, a disintegrant, an absorption promoter, a surfactant, an adsorption carrier and a lubricant.

10. The use of the active ingredient of Ganoderma lucidum in the preparation of a drug for treating myocardial ischemia according to claim 1, characterized in that: The medicine is an oral preparation or an injection.

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