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Article in English | WPRIM | ID: wpr-880558


OBJECTIVE@#Using network pharmacology to explore the mechanism of the 'invigorating qi and promoting blood circulation' drug pair Ginseng-Danshen (Salvia miltiorrhiza) on treatment of ischemic heart disease (IHD).@*METHODS@#The chemical constituents of ginseng and Danshen drug pair were identified by searching the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP), and the potential targets of the pair were identified. The pharmacodynamics of the pair was analyzed using network pharmacology. The targets of IHD were identified by database screening. Using protein-protein interaction network, the interaction targets of Ginseng-Danshen on IHD were constructed. A "constituent-target-disease" interaction network was constructed using Cytoscape software, Gene Ontology (GO) term enrichment analysis and biological pathway enrichment analysis were carried out, and the mechanism of improving myocardial ischemia by the Ginseng-Danshen drug pair was investigated.@*RESULTS@#Seventeen active constituents and 53 targets were identified from ginseng, 53 active constituents and 61 targets were identified from Danshen, and 32 protein targets were shared by ginseng and Danshen. Twenty GO terms were analyzed, including cytokine receptor binding, cytokine activity, heme binding, and antioxidant activity. Sixty Kyoto Encyclopedia of Genes and Genomes (KEGG) signaling pathways were analyzed, including phosphatidylinositol 3-kinase-serine-threonine kinase (PI3K-AKT) signaling pathway, p53 signaling pathway, interleukin 17 signaling pathway, tumor necrosis factor signaling pathway, and the advanced glycation end product (AGE)-the receptor for AGE (RAGE) signaling pathway in diabetic complications.@*CONCLUSION@#The specific mechanism of Ginseng-Danshen drug pair in treating IHD may be associated with improving the changes of metabolites inbody, inhibiting the production of peroxides, removing the endogenous oxygen free radicals, regulating the expression of inflammatory factors, reducing myocardial cell apoptosis and promoting vascular regeneration.

Article in Chinese | WPRIM | ID: wpr-872703


Objective:To observe the effect of oral administration of Tianlong Tongxin tablet on acute myocardial ischemia and related indexes in experimental dogs. Method:The model of acute myocardial ischemia in dogs was established and the dogs were divided into the control group (equal amount of normo-cyclodintrin 10 g·kg-1), Hexinshuang group (5 mg·kg-1), Tianlong Tongxin tablet high, medium and low dose groups (1, 0.5, 0.25 g·kg-1) and the compound Danshen tablet group (0.144 g·kg-1). Myocardial ischemia degree was measured by epicardium electrocardiogram, the range of myocardial infarction was determined by quantitative histology (N-BT staining), and coronary blood flow, cardiac output, myocardial oxygen consumption, coronary resistance and peripheral resistance were measured. Meanwhile, serum creatine kinase (CK), lactate dehydrogenase (LDH) and serum superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were detected by optical kit. Result:As compared with the control group, Tianlong Tongxin tablet can reduce the myocardial ischemia degree (∑-ST) measured by the electrocardiogram of the pericardium (P<0.05), reduce the infarcted area shown by N-BT staining (P<0.05), reduce the venous oxygen content (P<0.05), increase the coronary flow, cardiac output and myocardial oxygen consumption of anesthetized dogs, and reduce the coronary artery resistance and peripheral resistance (P<0.05). However, there was no significant difference in the influence of serum CK, LDH, SOD activity and MDA content in serum. Conclusion:Tianlong Tongxin tablet can improve acute myocardial ischemia and myocardial infarction in dogs.

Article in Chinese | WPRIM | ID: wpr-802164


Objective:To explore the protective effect of Tianlong Tongxin tablet on myocardial ischemia reperfusion injury in rats, and observe its effect on thrombosis, blood viscosity and platelet aggregation in rabbits. Method:Totally 56 Wistar rats were collected. Except for the sham operation group, all of the remaining rats were involved in the establishment of the rat myocardial ischemia reperfusion injury model. The successfully established model was divided model group, Hexinshuang group, compound Danshen tablet group and Tianlong Tongxin tablet groups (4, 2, 1 g·kg-1). Nitrotetrazolium blue (N-BT) method was used to observe the alleviation of myocardial infarction. Colorimetry was used to detect the effect of the test drug on serum superoxide dismutase (SOD) and malondialdehyde (MDA). The Chandler in vitro method was used to detect thrombosis and blood viscosity in vitro of control group, Tianlong Tongxin tablets groups (4, 2, 1 g·kg-1), compound Danshen tablets group and aspirin group. The Born turbidimetric method was used to observe the platelet aggregation levels of control group, Tianlong Tongxin tablets groups (2, 1, 0.5 g·kg-1), compound Danshen tablets group and aspirin group. Result:Compared with the sham operation group, the myocardial infarction area, serum SOD and MDA in the model group were significantly increased (PPP-1), compound Danshen tablets group and Aspirin tablets group could significantly shorten the length of thrombosis (PPPP-1 shear rates were significantly reduced (PP-1), compound Danshen tablet group and Aspirin tablet group (PPConclusion:Tianlong Tongxin tablet can protect rat myocardial ischemia reperfusion injury, inhibit platelet aggregation and thrombosis, and reduce blood viscosity.

Article in Chinese | WPRIM | ID: wpr-802054


Ischemic heart disease is one of the most deadly diseases in the world, and new therapies and preventive measures are urgently needed. In general, cardiomyocytes rely on adenosine triphosphate(ATP) produced by mitochondrial oxidative phosphorylation to maintain their systolic and ion pump functions. Autophagy is a procedural degradation mechanism widely present in eukaryotic cells. It is a self-defense mechanism and self-repair process of the body tissues. It is also a way of apoptosis and a basic phenomenon to maintain the energy balance of human cells. Mitochondrial autophagy is a type of selective autophagy in cells. In fact, damaged mitochondria selectively remove damaged proteins and organelles with autophagy to maintain intracellular homeostasis. Mitochondrial autophagy is important for maintaining the homeostasis of cardiomyocytes. With the deepening of modern biological research, more and more traditional Chinese medicines(TCM) or their extracts have been proven to alleviate myocardial cell damage after ischemia/reperfusion through autophagy or regulation of mitochondrial function. This further inspires TCM workers to find effective treatment measures by targeting mitochondria. Under the above background, this paper reviews the effects of mitochondrial autophagy on ischemic heart disease and the intervention studies of TCM in this field.

Article in Chinese | WPRIM | ID: wpr-773225


This study was to investigate the mechanism of safflower yellow injection for regulating inflammatory response against myocardial ischemia-reperfusion injury( MIRI) in rats. Male Wistar rats were randomly divided into sham operation group,model group,Hebeishuang group,safflower yellow injection high,medium and low dose groups. MIRI model was established by ligating left anterior descending coronary artery. Myocardial histopathological changes were observed by HE staining; myocardial infarct size was detected by TTC staining; content and changes of tumor necrosis factor-α( TNF-α) and interleukin-6( IL-6),serum creatine kinase( CK),aspartate aminotransferase( AST),and lactate dehydrogenase( LDH) were detected by biochemical method or enzyme-linked immunosorbent assay( ELISA). Western blot assay was used to detect the protein expression of Toll-like receptor 4( TLR4) and nuclear factor-κB( NF-κB p65) in myocardial tissues. The results showed that as compared with the sham operation group,the myocardial arrangement of the model group was disordered,with severe edemain the interstitial,significantly increased area of myocardial infarction,increased activities of AST,CK and LDH in serum,and significantly increased contents of TNF-α and IL-6; the expression levels of TLR4 and NF-κB( p65) protein in myocardial tissues were also increased. As compared with the model group,the myocardial tissues were arranged neatlyin the Hebeishuang group and safflower yellow injection high,medium and low dose groups; the edema was significantly reduced; the myocardial infarct size was significantly reduced; the serum AST,CK,LDH activity and TNF-α,IL-6 levels were significantly decreased,and the expression levels of TLR4 and NF-κB( p65) protein in myocardial tissues were decreased. As compared with the Hebeishuang group,the myocardial infarct size was larger in the safflower yellow injection high,medium and low dose groups; the activities of AST,CK and LDH in serum and the contents of TNF-α and IL-6 in serum were higher,but there was no statistically significant difference in the expression levels of TLR4 and NF-κB( p65) protein in tissues. It is suggested that safflower yellow injection has a significant anti-MIRI effect,and its mechanism may be related to the regulation of TLR-NF-κB pathway to inhibit inflammatory response.

Animals , Anti-Inflammatory Agents , Pharmacology , Aspartate Aminotransferases , Blood , Chalcone , Pharmacology , Creatine Kinase , Blood , Interleukin-6 , Metabolism , L-Lactate Dehydrogenase , Blood , Male , Myocardial Reperfusion Injury , Drug Therapy , Rats , Rats, Wistar , Toll-Like Receptor 4 , Metabolism , Transcription Factor RelA , Metabolism , Tumor Necrosis Factor-alpha , Metabolism