Fu Wen-yu, Chen Jia-ping, Wang Xiu-min, Xu Li-hong
Department of Biochemistry and Molecular Biology, School of Medicine, Zhejiang University, Hangzhou 310031, China.
Toxicon. 2005 Aug;46(2):171-7. doi: 10.1016/j.toxicon.2005.03.021.
It has been reported that MC-LR could induce apoptosis in a variety of cell types. Although the induction of oxidative stress and mitochondrial alteration played critical role in MC-LR induced apoptosis, but the exact mechanisms of MC-LR induced apoptosis are still unknown. In spite of extensive studies on MC-LR mediated cell damages, there is little information on the protein expression of p53 and Bcl-2, Bax in vivo and in vitro, which are vital regulator of apoptosis in response to a variety of stimuli. The present study was undertaken to determine the expression level of p53 and Bcl-2, Bax in cultured hepatocytes and rat liver tissues. The results show that MC-LR can increase the expression of p53 and Bax significantly both in vivo and in vitro, however, MC-LR can only decrease the expression of Bcl-2 significantly in vitro and there is no difference observed in vivo. It can be concluded that the expression of p53, Bcl-2 and Bax are involved in the regulation of MC-LR induced apoptosis.
据报道，微囊藻毒素-LR（MC-LR）可诱导多种细胞类型发生凋亡。尽管氧化应激的诱导和线粒体改变在MC-LR诱导的凋亡中起关键作用，但MC-LR诱导凋亡的确切机制仍不清楚。尽管对MC-LR介导的细胞损伤进行了广泛研究，但关于p53、Bcl-2和Bax在体内和体外的蛋白质表达情况知之甚少，而这些蛋白是响应多种刺激时凋亡的重要调节因子。本研究旨在确定培养的肝细胞和大鼠肝组织中p53、Bcl-2和Bax的表达水平。结果表明，MC-LR在体内和体外均可显著增加p53和Bax的表达，然而，MC-LR仅在体外可显著降低Bcl-2的表达，在体内未观察到差异。可以得出结论，p53、Bcl-2和Bax的表达参与了MC-LR诱导凋亡的调节。
