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《Journal of Clinical Internal Medicine》 2019-04
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Mechanism of TAGLN2 gene siRNA on lipopolysaccharide-induced apoptosis and oxidative damage of H9C2 cardiomyocytes

Yang Chunhua;Wang Ke;Wei Zhenheng;Niu Shaohui;Department of Cardiology, Zhoukou Central Hospital of Henan Province;  
Objective To investigate the effect of that TAGLN2 gene expression was inhibited on apoptosis and reactive oxygen species(ROS)level of H9C2 cardiomyocyte induced by lipopolysaccharide(LPS).Methods H9C2 cardiomyocyte were randomly divided into 4 groups:control group,LPS group,negative siRNA group and TAGLN2 siRNA group.SiRNA was transfected referred to Lipofectamine~(TM)2000.Western blotting was used to detect the expression of TAGLN2,nuclear factor(NF)-κB p65,p-NF-κB p65 and Bax protein.Cell viability was detected by cell counting kit 8(CCK8).Cell apoptosis rate and ROS level were detected by flow cytometry.Results The relative expression of TAGLN2 protein in H9 C2 cardiomyocyte decreased after TAGLN2 siRNA was transfect,which was significantly lower than that in control group(P0.05).Cell viability in LPS group was significantly lower than that in control group,apoptosis rate,ROS level and realtive expression of p-NF-κB p65 and Bax protein were significantly higher than those in control group(P0.05),but cell viability in TAGLN2 siRNA group was significantly higher than that in negative siRNA group,apoptosis rate,ROS level,relative expression of p-NF-κB p65 and Bax protein were significantly lower than those in negative siRNA group(P0.05).Conclusion Inhibition of TAGLN2 gene expression can reduce the apoptosis of H9C2 cardiomyocyte induced by LPS,which may be associated with decreased ROS level and down-regulation of NF-κB signal.
【Fund】: 河南省郑州市科技发展计划资助项目(20150110)
【CateGory Index】: R54
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