Protective effects of paeoniflorin against cobalt chloride-induced apoptosis of endothelial cells via HIF-1伪 pathway

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• 作者：Qiaoli Ji ; Lina Yang ; Jun Zhou ; Rong Lin ; ^{linrong63@yahoo.com.cn} ; Jiye Zhang ; Qinqin Lin ; Weirong Wang ; Kaifan Zhang
• 关键词：Paeoniflorin ; Cobalt chloride ; Hypoxia-inducible factor-1伪 ; Apoptosis ; Endothelial cells ; Atherosclerosis
• 刊名：Toxicology in Vitro
• 出版年：2012
• 期刊代码：48_08872333
• 类别：pha
• 出版时间：April, 2012
• 卷：26
• 期：3
• 页码：455-461
• 文件大小：455 K

摘要

Accumulating evidence has suggested the importance of hypoxia in the initiation and development of atherosclerotic lesion, and hypoxia has a profound impact on endothelial cell properties during cardiovascular disease processes. Paeoniflorin, isolated from the root of Paeonia lactiflora pall, can protect endothelial cells from hypoxic damage in a variety of ways, such as by enhancing the production of nitric oxide (NO) and decreasing the expressions of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). This study evaluated the protective effects of paeoniflorin against cobalt chloride (CoCl₂, a hypoxia-mimicking agent)-induced apoptosis of endothelial cells (CRL-1730) and the underlying mechanisms in vitro. Endothelial cells were exposed to CoCl₂ with or without pre-treatment with different concentrations of paeoniflorin. After treated with 0.6 mM CoCl₂ for 24 h, endothelial cells showed significant decrease in cell viability and increased apoptosis rate, which could be reversed by pre-treatment with paeoniflorin. Similarly, pre-treatment with paeoniflorin could prevent CoCl₂-induced hypoxia-induced factor-1伪 (HIF-1伪) accumulation and down-regulate the expressions of p53 and Bcl-2/adenovirus E1B 19 kDa interacting protein 3 (BNIP3). These findings indicate that paeoniflorin had effective protection against hypoxia-induced apoptosis of endothelial cells and that HIF-1伪, p53 and BNIP3 might be involved in this process.