【摘 要】
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Resveratrol (RES) protects myocardial cells from hypoxia/reoxygenation (H/R)-caused injury.However,the mechanism of this effect has not been clarified.Thus,in t
【机 构】
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Department of Cardiology, The People’s Hospital of Hunan Province, Changsha 410061, China;Department
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Resveratrol (RES) protects myocardial cells from hypoxia/reoxygenation (H/R)-caused injury.However,the mechanism of this effect has not been clarified.Thus,in this study,we aimed to determine whether RES attenuates H/R-induced cell necroptosis by inhibiting the tumor necrosis factor-alpha (TNF-α)/receptor-interacting protein kinase 1 (RIP1)/RIP3/mixed-lineage kinase domain-like (MLKL) signaling pathway.Rat myocardial ischemia/reperfusion (I/R) models and H/R-injured cell models were constructed.Our study showed that myocardial H/R injury significantly increased the levels of TNF-α,RIP1,RIP3,and p-MLKL/MLKL by western blot analysis.Cell viability assay and 4,6-dianmidino-2-phenylindole (DAPI)-propidium iodide staining showed that the cell viability was decreased,and necroptosis was increased after myocardial H/R injury.The expressions of TNF-α,RIP1,RIP3,and p-MLKL/MLKL in H/R myocardial cells treated with different concentrations of RES were significantly downregulated.In addition,we also found that the cell viability was increased and necroptosis was decreased in dose-dependent manners when H/R-injured cells were treated with RES.In addition,the enhanced effect of TNF-α on necroptosis in myocardial H/R-injured cells was improved by RES,and the effect of RES was confirmed in vivo in I/R rats.This study also showed that RES suppresses necroptosis in H9c2 cells,which may occur through the inhibition of the TNF-α/RIP1/RIP3/MLKL signaling pathway.Our data suggest that necroptosis is a promising therapeutic target and may be a promising therapeutic target for the treatment of myocardial I/R injury.
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