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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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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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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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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.