Acute myocardial infarction(AMI)is a common cardiovascular emergency in clinic.Early reperfusion is a typical and effective method for the treatment of AMI.However,the recovery of blood supply after reperfusion therapy will accelerate the damage of ischemic myocardium and cause myocardial ischemia-reperfusion injury(MI/RI).In recent years,studies have found that TCM has the unique advantages of multi-component,multi-channel and multi-target in the intervention of MI/RI.Janus tyrosine kinase/signal transducer and activator of transcription(JAK/STAT)signaling pathway is closely related to MI/RI,which can reduce MI/RI process by regulating inflammation,oxidative stress,cell proliferation,differentiation and apoptosis.This article reviewed the mechanism of JAK/STAT signaling pathway in MI/RI and the research of TCM targeting this pathway,in order to provide references for the prevention and treatment of MI/RI and further drug development.

Dilated cardiomyopathy is a main disease that causes heart failure and exhibits etiological heterogeneity.Nearly a quarter of dilated cardiomyopathy in patients is related to genetics,and ventricular dilation and myocardial systolic dysfunction are the main characteristics of the disease.LMNA mutation is a major cause of hereditary dilated cardiomyopathy,and arrhythmia is a major clinical manifestation of hereditary dilated cardiomyopathy with LMNA mutation.In recent years,establishment of a dilated cardiomyopathy model in C57/B6 mice and its treatment by focused gene therapy has been a research focus,and some important conclusion have been drawn from the establishment of large animal models in dogs and pigs.However,large animals,especially non-human primates,are closer to humans.At present,dilated cardiomyopathy is not involved in the heart disease model of non-human primates.Therefore,this article reviews studies on rodent and large animal models of dilated cardiomyopathy at the genetic level and proposes the idea of developing a dilated cardiomyopathy model in a non-human primate.It also provides new ideas to study the pathogenesis and clinical treatment.

Objective To clarify the intervention effect of Angelica Radix Astragali ultrafiltrate(RAS-RH)on radiation-induced myocardial fibrosis by inhibiting the overexpression of cardiac CILP1.Methods Forty SPF Wistar male rats were randomly divided into normal group,model group,Benazepril hydrochloride group,RAS-RH group and Benazepril hydrochloride +RAS-RH group.Cardiomyocytes were induced by X-ray.The rat model of myocardial fibrosis was prepared by injury.The benazepril hydrochloride group was given benazepril hydrochloride 1.0 mg·kg-1 by gavage;the RAS-RH group was given RAS-RH 0.6 g·kg-1 by gavage;benazepril hydrochloride was given by gavage Pril + RAS-RH group was given benazepril hydrochloride 1.0 mg·kg-1 and RAS-RH 0.6 g·kg-1 by gavage;model group and normal group were given equal volume of normal saline by gavage,once a day,After 4 weeks of drug intervention,the serum NT-ProBNP,CTnⅠ and CTnT contents of the rats in each group were detected by ELISA method;HE staining was used to evaluate the pathological changes of myocardial tissue of the rats in each group;Masson staining was used to evaluate the myocardial collagen deposition of the rats in each group and calculated Collagen volume fraction(CVF);immunohistochemistry to detect the expression levels of α-SMA,Col-Ⅰ,Col-Ⅲ protein in myocardial tissue of rats in each group;Western blot method to detect TGF-β1 and smad3 in myocardial tissue of rats in each group,CILP1 protein expression.Results Compared with the blank group,the serum levels of NT-ProBNP,CTnⅠ and CTnT in the model group were significantly increased(P<0.01).Blue-stained fibrous tissue increased significantly,myocardial CVF increased significantly,and myocardial tissue α-SMA,Col-Ⅰ,Col-Ⅲ,TGF-β1,Smad3,CILP1 protein expression increased(P<0.01);Serum contents of NT-ProBNP,cTnⅠ and CTnT in rats in napril group,RAS-RH group and benazepril hydrochloride + RAS-RH group were significantly decreased(P<0.01).Sexual cell infiltration was improved,myocardial CVF was significantly decreased(P<0.01),and the protein expressions of α-SMA,Col-Ⅰ,Col-Ⅲ,TGF-β 1,Smad3 and CILP1 in myocardial tissue were significantly decreased(P<0.05).Conclusion Angelica sinensis ultrafiltrate can alleviate X-ray radiation-induced myocardial fibrosis in rats by inhibiting the overexpression of CILP 1 in the heart.

Objective To observe the effects of Angelica Sinensis Radix and Astragali Radix extract(ASR-AR)on HUVEC pyroptosis;To explore its mechanism of treating coronary microvascular disease.Methods HUVEC were divided into blank group,model group,MCC950 group,ASR-AR low-,medium-and high-dosage groups.After modeling and treatment with drug containing serum,cell viability was detected by CCK-8 method,and cell apoptosis was detected by flow cytometry,phalloidin staining was used to detect cytoskeletal morphology,immunofluorescence staining was used to detect the expressions of VEGF,eNOS,Ang-2,ROS,ET-1 and TXA2,ELISA was used to detect the contents of IL-1β and IL-18 in cell supernatant,Western blot was used to detect the expressions of NLRP3,ASC,Caspase-1 and GSDMD protein in cells.Results Compared with the blank group,the model group showed a decrease in HUVEC cell viability(P<0.01)and an increase in cell apoptosis rate(P<0.01),cellular microfilament structure was in disorder and knotting,the expressions of VEGF and eNOS decreased,and expressions of Ang-2,ROS,ET-1 and TXA2 increased,the contents of IL-1β and IL-18 in cell supernatant increased(P<0.01),and the expressions of NLRP3,ASC,Caspase-1 and GSDMD protein in cells increased(P<0.01).Compared with the model group,ASR-AR low-,medium-and high-dosage containing serum could increase cell viability(P<0.05),decrease cell apoptosis rate(P<0.05),improve cell microfilament structure,elevate VEGF and eNOS expressions,decrease Ang-2,ROS,ET-1,TXA2 expressions,reduce IL-1β and IL-18 contents in cell supernatant(P<0.05),and decrease NLRP3,ASC,Caspase-1 and GSDMD protein expressions(P<0.05).ASR-AR medium-dosage group was more obvious(P<0.05).Conclusion ASR-AR can inhibit pyroptosis of HUVEC induced by AngⅡ,attenuate endothelial cell dysfunction,thus treating coronary microvascular disease,and its mechanism may be related to the inhibition of the assembly of NLRP3 inflammasome.

Myocardial infarction （MI） is a common cardiovascular disease in clinical practice and one of the main causes of cardiovascular mortality. Its pathogenesis is complex and associated with oxidative stress reactions. Nuclear factor E₂-related factor 2 （Nrf2） is a key factor in regulating oxidative stress reactions. It can regulate the expression of heme oxygenase-1 （HO-1）， playing a role in maintaining the oxidative-reductive homeostasis in the body. During the course of MI， the biological activity and levels of Nrf2 and HO-1 decrease， leading to weakened tissue antioxidant and anti-inflammatory capabilities， endothelial damage in myocardial blood vessels， release of vascular cell adhesion factors， and impaired endothelial function. In recent years， many basic research studies have explored the role and mechanisms of traditional Chinese medicine （TCM） in treating MI by modulating the Nrf2/HO-1 signaling pathway. The results have indicated that the Nrf2/HO-1 signaling pathway is an important potential target for TCM in the treatment of MI. This article reviewed the mechanism of the Nrf2/HO-1 signaling pathway in MI and the research progress of TCM in targeting and regulating this pathway， aiming to provide a theoretical basis for the prevention and treatment of MI and further drug development.

AIM: To reveal that the targeted regulation of TGF-β1 by miR-21-5P is the key mechanism that mediates the activation of myocardial fibroblasts, and to clarify the intervention ofRadix Angelica Sinensis and Radix Hedysari ultrafiltration on the mechanism of miR-21-5P targeting to regulate TGF-β1 effect. METHODS: (1) The cells were randomly divided into normal group and irradiation group. The irradiation group received 6Gry single irradiation, and then RT-PCR was used to detect miR-21-5P, and Western Blot was used to detect the expression of α-SMA and TGF-β1. (2) The cells were randomly divided into normal group, irradiation group, miR-21-5P

Myocardial injury is a pathological change of myocardium caused by many factors,which can lead to the decline of cardiac function and the occurrence of cardiovascular events.Astragaloside Ⅳ is one of the main pharmacological components in Astragali Radix,which plays an anti-myocardial injury role by regulating various signaling pathways.This article reviewed the anti-myocardial injury mechanism of astragaloside Ⅳ from five aspects:inhibition of oxidative stress,inhibition of apoptosis,anti-myocardial fibrosis,improvement of myocardial energy metabolism and inhibition of myocardium inflammation,in order to provide reference for the mechanism research and clinical application of astragaloside Ⅳ in the prevention and treatment of myocardial injury.

AIM:To explore the potential targets and mechanisms of Angelica sinensis and Astraga-lus membranaceus ultrafiltration(RAS-AM)in the treatment of radiation induced myocardial fibrosis(RIMF)through network pharmacology combined experimental validation.METHODS:Using the TC-MSP database TCM@TAIWAN The Taiwan Tradition-al Chinese Medicine Database and TCMID Tradition-al Chinese Medicine Database screen the compo-nents and targets of RAS-AM,and use the Swiss Target Prediction database for target prediction.Obtain RIMF disease targets from Gene Cards and OMIM databases,obtain intersection targets of dis-eases and drugs through Wayne's online tool,ob-tain protein interaction relationships(PPIs)through STRING database,and use Cytoscape 3.9.1 soft-ware to construct a visualized network topology di-agram of"drug component target disease".Con-duct GO and KEGG enrichment analysis on core tar-gets through the David database,and use the mi-crobiome platform for mapping.Experimental veri-fication:Sixty Wistar rats were randomly divided in-to a blank group,a model group,a positive drug group,a RAS-AM low-dose group,a RAS-AM medi-um dose group,and a RAS-AM high-dose group.A RIMF model was established using a 38Gy dose of radiation induction,and was administered orally for 4 weeks.The general condition of the rats was also observed.After blood and heart collection in rats,HE staining was used to observe the morpho-logical changes of myocardial tissue,and ELISA and Western blot methods were used to detect key tar-gets for network pharmacology prediction.RE-SULTS:Network pharmacology analysis revealed 34 active components and 705 targets of Angelica si-nensis and Astragalus membranaceus ultrafiltra-tion,with a total of 154 targets,with IL-6,VEGFA,MMP2,MMP9,and ACE as the top five core tar-gets;GO enrichment analysis screened a total of 153 entries,and KEGG enrichment had 25 path-ways.Experimental part:HE staining results showed that the degeneration and necrosis of myo-cardial cells improved in each medication group,the infiltration of inflammatory cells in the myocar-dial interstitium decreased,and the proliferation of fibrous connective tissue in the myocardial intersti-tium decreased.ELISA and Western blot results showed that compared with the normal group,the expression of IL-6,VEGFA,and MMP-9 in the mod-el group increased.Compared with the model groupthe expression of IL-6,VEGFA,and MMP-9 in each medication group decreased to varying de-grees,in a dose-dependent manner.CONCLUSION:RAS-AM may inhibit RIMF by downregulating core targets such as IL-6,VEGFA protein,MMP-9 pro-tein,and regulating inflammatory pathways,colla-gen degradation,and other processes.

AIM: To study the mechanism of Ginseng Yixin granules (QSYXG) in treating ejection fraction preserved heart failure (HFpEF) based on network pharmacology. METHODS: Effective chemical composition information of QSYXG particles was collected through TCMSP database; DisGeNET, GeneCards, OMIM database for obtaining HFpEF related targets; Metascape GO and KEGG enrichment analysis of the intersection targets of HFpEF; STRING Construction and analysis of the database PPI network; Cytoscape3.7.2 Software construction network diagram; Docking of the major active components to the core target with the AutoDock Vina software molecules, the results were visualized and analyzed with pymol. RESULTS: A total of 66 components and corresponding targets were obtained, HFpEF corresponds to 1 931 targets, The intersection of 127 targets, the main active ingredients are quercetin, kaempferol, β-sitosterol, etc.; TNF, AKT1, IL-6, P53 and JUN as the core targets, Good docking of the key components with the core targets; Mainly involving the positive regulation of gene expression, signal transduction, negative regulation of apoptotic process, positive regulation of cell proliferation and senescence, hypoxia response, negative regulation of gene expression, inflammatory response and so on, PI3K-Akt, AGE-RAG, MAPK, TNF, IL-17, and HIF-1 are the main associated signaling pathways. CONCLUSION: QSYXG may treat HFpEF by activating targets of TNF, AKT1, IL-6, P53, JUN, and regulating apoptotic process, cell proliferation, hypoxia response, and inflammatory response.

Heart failure is a common frequently-occurring disease, and it is the terminal stage of the development of various heart diseases. The pathogenesis is very complex and seriously endangers human health. A large number of studies have shown that Ca2+/Calmodulin dependent protein kinase II(CaMKII) plays an important role in the occurrence and development of heart failure. Traditional Chinese medicine has unique advantages and good prospects in the prevention and treatment of heart failure. Among them, there are many compound and their active ingredients can target and regulate CaMKII. This paper mainly expounds the mechanism of the CaMKII signaling pathway in the failing heart and the research progress of traditional Chinese medicine in preventing and treating heart failure by targeting the regulation of CaMKII signaling in recent years, in order to provide reference and expand ideas for clinical traditional Chinese medicine prevention and treatment in heart failure.