Lan Hong, Lü You-yong
Beijing Molecular Oncology, Beijing Institute for Cancer Research, School of Oncology, Peking University, Beijing 100034, China.
Acta Pharmacol Sin. 2004 Feb;25(2):219-25.
To investigate the mechanism of allitridi-induced apoptosis in human gastric cancer cell line BGC823.
Growth inhibition by allitridi was analyzed using cell growth curve and MTT assay. Apoptotic cells were detected using staining with Hoechst 33342, and confirmed by flow cytometric analysis and DNA fragmentation analysis. The protein expression affected by allitridi was determined using Western blot. The activity of caspase-3 was measured using a fluorescence assay.
Allitridi induced apoptosis, and then inhibited cells proliferation in human gastric cancer cell line BGC823. The protein level of Bcl-2 was decreased dramatically, while Bax and p53 were not significantly affected by allitridi. The expression and activity of caspase-3 started to increase after allitridi treatment for 72 h.
Allitridi induced apoptosis through down-regulation of Bcl-2, and increased caspase-3 expression and its activity.
探讨大蒜素诱导人胃癌细胞系BGC823凋亡的机制。
采用细胞生长曲线和MTT法分析大蒜素对细胞生长的抑制作用。用Hoechst 33342染色检测凋亡细胞，并通过流式细胞术分析和DNA片段化分析进行确认。用蛋白质免疫印迹法测定大蒜素影响的蛋白质表达。用荧光法测定caspase-3的活性。
大蒜素诱导人胃癌细胞系BGC823凋亡，进而抑制细胞增殖。Bcl-2蛋白水平显著降低，而Bax和p53不受大蒜素的显著影响。大蒜素处理72小时后，caspase-3的表达和活性开始增加。
大蒜素通过下调Bcl-2诱导凋亡，并增加caspase-3的表达及其活性。
