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

    標題: San-Huang-Xie-Xin-Tang protects cardiomyocytes against hypoxia/reoxygenation injury via inhibition of oxidative stress-induced apoptosis
    作者: Liou, Shu-Fen
    Hsu, Jong-Hau
    Liang, Jyh-Chong
    Ke, Hung-Jen
    Chen, Ing-Jun
    Wu, Jiunn-Ren
    Yeh, Jwu-Lai
    貢獻者: 藥學系
    關鍵字: San-Huang-Xie-Xin-Tang
    Reactive Oxygen Species
    日期: 2012-04
    上傳時間: 2014-03-21 16:17:05 (UTC+8)
    出版者: Springer Tokyo
    摘要: 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.
    Appears in Collections:[藥學系(所)] 期刊論文

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