Journal of
Medicinal Plants Research

  • Abbreviation: J. Med. Plants Res.
  • Language: English
  • ISSN: 1996-0875
  • DOI: 10.5897/JMPR
  • Start Year: 2007
  • Published Articles: 3834

Full Length Research Paper

Hypaconitine protects H9c2 cells from oxidative stress-induced apoptosis

Zhi-Hui Li1, Wanhong Xu2, Guo-Hui Li1, Ling Shen3, Min-Jie Mao1, Zhi-Gang Wu3, Xue-Ting Shao3 and Kun Fang1*
1Department of Intensive Care Unit, Hangzhou Red Cross Hospital, Zhejiang Chinese Medical University, China. 2Hangzhou High Throughput Drug Screening Center, ACEA Bio, Hangzhou, Zhejiang, China. 3State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, the First Affiliated Hospital, Zhejiang University School of Medicine, China.
Email: [email protected]

  •  Accepted: 18 November 2011
  •  Published: 09 February 2012


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


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