miR-330-5p Protection Myocardial Ischemia Reperfusion by Inhibiting MAPK Pathway
Objective:To investigate the mechanism of miR-330-5p to protect myocardial ischemia reperfusion and its influence on mitogen activated protein kinase(MAPK)signaling pathway.Methods:Human cardiac myocyte AC 16 was cultured in vitro,and miR-330-5p mimic was transfected into AC 16 cells.To establish a myocardial ischemia reperfusion model in vitro,cells were cultured in 1％O2+5％CO2+94％N2 condition to build a cardiomyocyte oxygen and glucose deprivation/reoxygenation(OGD/R)model.Cell apoptosis rate was detected by flow cytometry,and ELISA was performed to detect the concentrations of 4-hydroxynonenal(4-HNE)and Malondialdehyde(MDA).The protein expression of Bcl-2 associated X protein(Bax)and B-cell lymphoma-2(Bcl-2),Aldehyde dehydrogenase 2(ALDH2)and key proteins of MAPK pathway,extracellular regulated protein kinases(ERK1/2),C-jun N-terminal kinasei(JNK1)and p38 mitogen activated protein kinase(p38 MAPK)were detected by Western Blot assay.Results:In OGD/R model,the apoptosis rate of cardiac myocytes was increased,and the secretion of 4-HNE and MDA were increased significantly,while ALDH2 was deceased.For apoptosis markers,Bax was increased while Bcl-2 was decreased significantly.After miR-330-5p mimic transfection,4-HNE and MDA were significantly decreased,and ALDH2 was increased.Cell apoptosis was significantly decreased.As for MAPK signaling pathway,ERK1/2,JNK1 and p38 MAPK were decreased by miR-330-5p mimic.Conclusion:MiR-330-5p can regulate ALDH2 expression by inhibiting MAPK signaling pathway,and inhibits oxidative stress and apoptosis of cardiac myocyte during myocardial ischemia reperfusion,so as to protect myocardial cells.
miR-330-5pMyocardial reperfusion injuryMitogen-activated protein Kinase KinasesOxidative stress
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