Accepted for publication Sep 18, 2021.Ĭardiovascular disease (CVD) is a public health crisis that accounts for >30% of all deaths globally ( 1).
WESTERN BLOT RESULTS CARDIOMYOCYTES ACTIVATOR
Keywords: H9c2 hypoxia astragaloside IV (AS-IV) hypoxia-inducible factor 1α ( HIF-1α) Janus kinase 2/signal transducer and activator of transcription 3 signaling ( JAK2/STAT3 signaling) The beneficial functions of AS-IV in hypoxia-exposed H9c2 cells were linked to HIF-1α upregulation and JAK2/STAT3 signaling activation.Ĭonclusions: AS-IV relieved H9c2 cardiomyocyte injury after hypoxia, possibly by activating JAK2/STAT3-mediated HIF-1α signaling. AS-IV promoted JAK2/STAT3 signaling in hypoxia-induced injury.
Downregulation of HIF-1α suppressed the function of AS-IV in hypoxia-challenged H9c2 cells. Moreover, HIF-1α signaling was further activated and stabilized by AS-IV in hypoxia-challenged H9c2 cells. AS-IV eliminated hypoxia-induced H9c2 injury. Results: Hypoxia suppressed viability and promoted the apoptosis and death of H9c2 cells. Furthermore, the regulatory role of Janus kinase 2/signal transducer and activator of transcription 3 ( JAK2/STAT3) signaling on HIF-1α levels was examined. Next, transfection of si- HIF-1α into H9c2 cells was carried out to test whether upregulation and stabilization of HIF-1α influences the effect of AS-IV on hypoxia-treated H9c2 cells. Cell apoptosis, death, and viability as well as hypoxia-inducible factor 1α ( HIF-1α) expression and apoptotic proteins were analyzed. Methods: First, H9c2 cells were exposed to hypoxia and/or AS-IV treatment. Here, the effect of AS-IV on hypoxia-injured H9c2 cardiomyocytes was elucidated. Astragaloside IV (AS-IV) is the main component of Astragalus membranaceus and could exert cardiac protective role. Policy of Dealing with Allegations of Research Misconductīackground: Hypoxia is an important cause of myocardial injury due to the heart’s high susceptibility to hypoxia.Policy of Screening for Plagiarism Process.New insights into the role of mitochondria in cardiac microvascular ischemia/reperfusion injury. Value of primordial and primary prevention for cardiovascular disease. Myocardial protection from ischemia-reperfusion injury post coronary revascularization. Journal of the American College of Cardiology. Universal definition of myocardial infarction. This might be the reason why SMYAD protected myocardial tissue and improved cardiac function in mice with ischemia/reperfusion. SMYAD exerted protective effects on ischemia/reperfusion injury in myocardial cells by activating autophagy and inhibiting pyroptosis. SMYAD elevated the rate of LC3B-II/LC3B-I protein expression, decreased the rate of p-mTOR/mTOR protein expression, and reduced expressions of caspase 1, NLRP3, and IL-1 β in H/R cardiomyocytes. SMYAD improved the survival rate of H9C2 cardiomyocytes in the H/R injury model. It was found that SMYAD could regulate collagen I, MMP9, and TNF α protein expression levels in the heart tissues. Morphological assay indicated that SMYAD reduced the scar size and inhibited fibrosis formation. SMYAD improved cardiac functions such as ventricular volume and ejection fraction of the rats with ischemia/reperfusion injury. The expression levels of LC3B-II/LC3B-I, p-mTOR, mTOR, NLRP3, procaspase 1, and cleaved-caspase 1 in H9C2 cells were evaluated by Western blot. The expression level of IL-1 β was evaluated by ELISA. MTT assays detected the cell viability of myocardial cells. H9C2 cells were used to establish the hypoxia/reoxygenation (H/R) model and SMYAD intervention. The protein expression of collagen I, MMP9, and TNF α was detected by western blot in the heart tissues. Histopathological analysis for the heart remodeling was detected by H&E and Masson staining. Then, the cardiac functions of mice were evaluated by cardiac magnetic resonance (CMR). The aim of this study was to determine whether Si-Miao-Yong-An decoction (SMYAD) could protect cardiomyocytes from ischemia/reperfusion (I/R) injury and its underlying mechanisms.Ĭ57BL/6 mice were used to establish a model of myocardial infarction by I/R injury and treated by SMYAD for 4 weeks.
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