San-Huang-Xie-Xin-Tang protects cardiomyocytes against hypoxia/reoxygenation injury via inhibition of oxidative stress-induced apoptosis

doi:10.1007/s11418-011-0592-0

CNU IR > Pharmacy and Science > Dept. of Pharmacy > Periodical Articles > Item 310902800/27669

Please use this identifier to cite or link to this item: https://ir.cnu.edu.tw/handle/310902800/27669

Title:	San-Huang-Xie-Xin-Tang protects cardiomyocytes against hypoxia/reoxygenation injury via inhibition of oxidative stress-induced apoptosis
Authors:	Liou, Shu-Fen Hsu, Jong-Hau Liang, Jyh-Chong Ke, Hung-Jen Chen, Ing-Jun Wu, Jiunn-Ren Yeh, Jwu-Lai
Contributors:	藥學系
Keywords:	San-Huang-Xie-Xin-Tang Hypoxia/Reoxygenation Reactive Oxygen Species Apoptosis Enos Cardioprotection
Date:	2012-04
Issue Date:	2014-03-21 16:17:05 (UTC+8)
Publisher:	Springer Tokyo
Abstract:	Oxidative stress has been widely implicated in the pathogenesis of hypoxia/reoxygenation (H/R) injury. San-Huang-Xie-Xin-Tang (SHXT), a widely used traditional Chinese medication, has been shown to possess antioxidant effects. Here, we investigated whether SHXT and its main component baicalin can attenuate oxidative stress induced by H/R injury. H9c2 rat ventricular cells were exposed to SHXT or baicalin followed by hypoxia for 24 h and/or reoxygenation for 8 h. Pretreatment with SHXT and baicalin both significantly prevented cell death and production of reactive oxygen species induced by hypoxia or H/R in H9c2 cardiomyoctes. In addition, SHXT and baicalin also inhibited hypoxia- or H/R-induced apoptosis, with associated decreased Bax protein, increased Bcl-2 protein, and decreased caspase-3 activity. Furthermore, we found that hypoxia and H/R decreased endothelial nitric oxide synthase (eNOS) expression and nitrite production, and these effects were counteracted by SHXT and baicalein. Finally, SHXT inhibited H/R-induced activation of p38 mitogen activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK) phosphorylation in H9c2 rat ventricular cells. The present study demonstrates for the first time that SHXT can protect cardiomyocytes from H/R injury via inhibition of oxidative stress-induced apoptosis. These cardioprotective effects are possibly mediated through eNOS enhancement and p38 MAPK and JNK-dependent signaling pathways.
Relation:	Journal of Natural Medicines, 66(2), 311-320
Appears in Collections:	[Dept. of Pharmacy] Periodical Articles

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