Hypaconitine protects H9c2 cells from oxidative stress-induced apoptosis

• DOI: 10.5897/jmpr11.1467
• Publication Date: 2012-02-16T03:21:04Z
• Authors: Zhi-Hui Li
• Keywords: 01 natural sciences; 0104 chemical sciences; 3. Good health

The aim of the present study was to investigate protective effect hypaconitine on apoptosis induced by H2O2 and underlying molecular mechanism in cardiac myocytes. First, myocytes were pretreated with different concentrations (0, 62.5, 125, and 250 ng/ml) before exposure 100 µM H2O2. Cell viability, apoptosis, activation caspase-3 -9, p38 mitogen-activated protein kinases (MAPK), nuclear factor κB (NF-κB) p65 examined. In our study, H2O2 treatment resulted a dose-dependent increase number apoptotic cells. addition, total phorspho-p38 MAPK phorspho-NF-κB p65, measured western blot, markedly activated and, H2O2 was significantly reduced pretreatment manner. Similarly, MAPK, blocked hypaconitine; strongest observed at ng/ml. conclusion, this we first demonstrated that protects from triggered H2O2 in manner ranging 62.5 results, least partially, showed inhibited cell via blocking 3 important signaling pathways, pathway, NF-κB caspase mediated H2O2.

Key words: Oxidative stress, heart failure, H9c2, hypaconitine.