Icariin protects against ischemia-reperfusion injury in H9C2 cells by upregulating heat shock protein 20.

Icariin (ICA) has been implicated in certain biological and pathological processes, including myocardial ischemia/reperfusion (I/R) injury. The aim of the present study was to investigate the role of ICA in I/R-induced cardiomyocyte injury and the potential underlying mechanism. Cell proliferation and apoptosis of H9C2 cells was determined by cell counting kit-8 and flow cytometry assays. In addition, reactive oxygen species (ROS) production in H9C2 cells was measured by flow cytometry. Reverse transcription-quantitative polymerase chain reaction and western blot assay were performed to examine the expression levels of proteins, including HSP20, B-cell lymphoma 2 (Bcl-2), cytochrome complex (Cyt-c), apoptotic protease activating factor 1 (APAF1), caspase-9 andcaspase-3, and the phosphorylation of Akt (p-Akt) in H9C2 cells. The present results demonstrated that, compared with the control group, the I/R group demonstrated significantly reduced levels of HSP20 expression and cell proliferation, and increased apoptosis and ROS production in H9C2 cells. In parallel, the expression levels of Cyt-c, APAF1, caspase-9 and caspase-3 were significantly increased in the I/R group, although Bcl-2 and p-Akt/Akt expression levels were decreased. Furthermore, compared with the I/R group, ICA treatment and/or HSP20 overexpression significantly improved cardiac function, as evidenced by promoted cell proliferation and inhibited apoptosis of H9C2 cells. The current study indicates that ICA exerts a cardioprotective effect against I/R injury, which is associated with the upregulation of HSP20. [ABSTRACT FROM AUTHOR]