Inhibition of iNOS protects cardiomyocytes against coxsackievirus B3-induced cell injury by suppressing autophagy

Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie
Li QiJia Wenjun

Abstract

Coxsackievirus B3 (CVB3), a member of the picornavirus family, is one of the major causative enteroviruses of viral myocarditis. The aim of the current study was to investigate the role and underlying mechanism of iNOS and autophagy in CVB3 infected cardiomyocytes. Myocardial cell H9c2 were randomly divided into four groups: control group, CVB3 group, CVB3+L-NAME group and the CVB3+iNOS siRNA group. Cell proliferation was detected by MTT method and cell apoptosis was determined by flow cytometric. The protein expression levels were determined by Western blot. Anisomycin was used to activate JNK pathway in CVB3 infected H9c2 cells. The results demonstrated that the inhibition of iNOS significantly elevated cell proliferation and suppressed cell apoptosis of CVB3-induced H9c2 cells. The production of MDA was obviously decreased, while the activity of SOD was increased by the addition of L-NAME or iNOS siRNA compared with the CVB3 group. Expression of the autophagy marker proteins LC3 II and Beclin 1 was significantly decreased, and the autophagy substrate p62 was dramatically increased in iNOS inhibition groups compared with the CVB3 group. Moreover, iNOS inhibition suppressed the JNK pathway in CVB3-infected H9c2 cells. Furtherm...Continue Reading

Citations

Jun 1, 2018·BioMed Research International·Chunmiao LuJunping Zhang
Dec 16, 2019·Biochemical and Biophysical Research Communications·Ji-Ying ChenYuan Guo
Jul 14, 2021·Scientific Reports·Michael F BodeNigel Mackman

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