Kuo Po-Lin, Hsu Ya-Ling, Cho Chien-Yu, Ng Lean-Teik, Kuo Yueh-Hsiung, Lin Chun-Ching
Department of Biotechnology, Chia-Nan University of Pharmacy and Science, Tainan, Taiwan.
Food Chem Toxicol. 2006 Aug;44(8):1316-26. doi: 10.1016/j.fct.2006.02.009. Epub 2006 Feb 28.
Antrodia cinnamomea is well known in Taiwan as a traditional medicine for treating cancer and inflammation. The purpose of this study was to evaluate the apoptotic effects of ethylacetate extract from A. cinnamomea (EAC) fruiting bodies in Hep 3B, a liver cancer cell line. EAC decreased cell proliferation of Hep 3B cells by inducing apoptotic cell death. EAC treatment increased the level of calcium (Ca2+) in the cytoplasm and triggered the subsequent activation of calpain and caspase-12. EAC also initiated the mitochondrial apoptotic pathway through regulation of Bcl-2 family proteins expression, release of cytochrome c, and activation of caspase-9 in Hep 3B cells. Furthermore, the mitochondrial apoptotic pathway amplified the calpain pathway by Bid and Bax interaction and Ca2+ translocation. We have therefore concluded that the molecular mechanisms during EAC-mediated proliferation inhibition in Hep 3B cells were due to: (1) apoptosis induction, (2) triggering of Ca2+/calpain pathway, (3) disruption of mitochondrial function, and (4) apoptotic signaling being amplified by cross-talk between the calpain/Bid/Bax and Ca2+/mitochondrial apoptotic pathways.
牛樟芝在台湾作为治疗癌症和炎症的传统药物而闻名。本研究的目的是评估牛樟芝子实体乙酸乙酯提取物（EAC）对肝癌细胞系Hep 3B的凋亡作用。EAC通过诱导凋亡性细胞死亡降低了Hep 3B细胞的增殖。EAC处理增加了细胞质中钙（Ca2+）的水平，并引发了随后钙蛋白酶和半胱天冬酶-12的激活。EAC还通过调节Bcl-2家族蛋白表达、细胞色素c的释放以及Hep 3B细胞中半胱天冬酶-9的激活启动了线粒体凋亡途径。此外，线粒体凋亡途径通过Bid和Bax相互作用以及Ca2+转运放大了钙蛋白酶途径。因此，我们得出结论，EAC介导的Hep 3B细胞增殖抑制过程中的分子机制是由于：（1）凋亡诱导，（2）Ca2+/钙蛋白酶途径的触发，（3）线粒体功能的破坏，以及（4）钙蛋白酶/Bid/Bax和Ca2+/线粒体凋亡途径之间的相互作用放大了凋亡信号。
