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

Abstract

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.