Li Pei-Pei, He Wei, Yuan Ping-Fan, Song Sha-Sha, Lu Jing-Tao, Wei Wei
Institute of Clinical Pharmacology, Anhui Medical University, Hefei 230032, Anhui, P.R. China.
Am J Chin Med. 2015;43(1):137-48. doi: 10.1142/S0192415X15500093. Epub 2015 Feb 5.
Celastrol is a natural terpenoid isolated from Tripterygium wilfordii, a well-known Chinese medicinal herb that presents anti-proliferative activities in several cancer cell lines. Here, we investigated whether celastrol induces apoptosis on hepatocellular carcinoma Bel-7402 cells and further explored the underlying molecular mechanisms. Celastrol caused a dose- and time-dependent growth inhibition and apoptosis of Bel-7402 cells. It increased apoptosis through the up-regulation of Bax and the down-regulation of Bcl-2 in Bel-7402 cells. Moreover, celastrol induced the release of cytochrome c and increased the activation of caspase-3 and caspase-9, suggesting that celastrol-induced apoptosis was related to the mitochondrial pathway. These results indicated that celastrol could induce apoptosis in Bel-7402 cells, which may be associated with the activation of the mitochondria-mediated pathway.
雷公藤红素是从著名的中草药雷公藤中分离出的一种天然萜类化合物,它在多种癌细胞系中具有抗增殖活性。在此,我们研究了雷公藤红素是否能诱导人肝癌Bel-7402细胞凋亡,并进一步探讨其潜在的分子机制。雷公藤红素对Bel-7402细胞产生剂量和时间依赖性的生长抑制及凋亡作用。它通过上调Bel-7402细胞中Bax的表达及下调Bcl-2的表达来增加细胞凋亡。此外,雷公藤红素诱导细胞色素c的释放,并增强caspase-3和caspase-9的激活,这表明雷公藤红素诱导的细胞凋亡与线粒体途径有关。这些结果表明,雷公藤红素可诱导Bel-7402细胞凋亡,这可能与线粒体介导途径的激活有关。