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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.
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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.
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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.
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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.
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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.
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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.
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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
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Objective To observe the effects of ShenGuiBaoXin decoction on matrix metalloproteinases-2 (MMP-2), the tissue inhibitor of matrix metalloproteinase-1 (TIMP-1), brain natriuretic peptide (BNP) levels, and cardiac histopathology in rats with heart failure, and to investigate the mechanism of the inhibition effect on ventricular remodeling in rats with heart failure. Methods Ninety male SD rats were randomly divided into two groups, with 15 rats in the control group and 75 rats in the model group. Normal saline was injected in the normal control group. The model group was given an intraperitoneal injection of isoprenaline 3 mg/ (kg·d). After 4 weeks, an ejection fraction of ≤50％ on echocardiography was considered a successful model. Seventy-five rats were randomly divided into the model, Qiliqiangxin, and ShenGuiBaoXin groups (high, medium, and low doses), with 15 rats in each group. Eight weeks later, the cardiothoracic ratio and BNP level were measured, hematoxylin-eosin staining was performed, and the MMP-2 and TIMP-1 protein expressions in the myocardium was detected. Results In terms of cardiothoracic ratio and BNP level, all the groups showed decreases after treatment, especially the Qiliqiangxin and high-dose groups. The MMP-2 protein expression level was decreased in all the groups after the treatment, and the high-dose group was superior to the Qiliqiangxin group. Conclusion ShenGuiBaoXin decoction functions by reducing the MMP-2 expression level, regulating MMP-2/TIMP-1 dynamic balance, maintaining the balance of synthesis and degradation of the extracellular matrix, inhibiting ventricular remodeling, and improving cardiac function.
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BACKGROUND: Chinese herbal medicine has been used to treat hypertension in China and East Asia since centuries. In this study, we conduct an overview of systematic reviews of Chinese herbal medicine in the treatment of primary hypertension to 1) summarize the conclusions of these reviews, 2) evaluate the methodological quality of these reviews, and 3) rate the confidence in the effect on each outcome. METHODS: We comprehensively searched six databases to retrieve systematic reviews of Chinese herbal medicine for primary hypertension from inception to December 31, 2015. We used AMSTAR to evaluate the methodological quality of included reviews, and we classified the quality of evidence for each outcome in included reviews using the GRADE approach. RESULTS: A total of 12 systematic reviews with 31 outcomes were included, among which 11 systematic reviews focus on the therapeutic effect of Chinese herbal medicine combined with conventional medicine or simple Chinese herbal medicine versus simple conventional medicine. Among the 11 items of AMSTAR, the lowest quality was "providing a priori design" item, none review conformed to this item, the next was "stating the conflict of interest" item, only three reviews conformed to this item. Five reviews scored less than seven in AMSTAR, which means that the overall methodological quality was fairly poor. For GRADE, of the 31 outcomes, the quality of evidence was high in none (0 %), moderate in three (10 %), low in 19 (61 %), and very low in nine (29 %). Of the five downgrading factors, risk of bias (100 %) was the most common downgrading factor in the included reviews, followed by imprecision (42 %), inconsistency (39 %), publication bias (39 %), and indirectness (0 %). CONCLUSIONS: The methodological quality of systematic reviews about Chinese herbal medicine for primary hypertension is fairly poor, and the quality of evidence level is low. Physicians should be cautious when applying the interventions in these reviews for primary hypertension patients in clinical practice.
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Drugs, Chinese Herbal/therapeutic use , Essential Hypertension/drug therapy , Research Design/standards , Review Literature as Topic , Humans , Medicine, Chinese Traditional , Publication BiasABSTRACT
Objective: To explore the relationship between ambulatory arterial stiffness indexes (AASI), AASI-blood pressure variability (AASI-BPVR) and left ventricular mass index (LVMI) left atrium diameter (LAD) in patients with hypertension. Methods: A total of 286 hypertensive patients were enrolled in this study. The AASI, AASI-BPVR were calculated from 24-hour ambulatory blood pressure monitoring. Left ventricular internal dimension in diastole (LVIDd), interventricular septal thickness in diastole (IVSd), posterior wall thickness in diastole (PWd), LAD were detected by echocardiography and LVMI, relative wall thickness (RWT) were calculated. The fasting blood glucose, blood lipids were examined. According to 24 h AASI, the patients were divided into 2 groups, Group A, the patients with AASI > 0.51, n=133 and Group B, the patients with AASI ≤ 0.51,n=153. Pearson and multi regression analysis were conducted to analyze the relevant correlations. Results: Group A had increased LVMI than that in Group B,P Conclusion: AASI and AASI-BPVR were not the independent factors for left ventricular hypertrophy and left atrial enlargement, therefore, they were not the predictors for cardiac damage in patients with hypertension at present time.