N-马来酰-L-缬氨酸酯姜黄素诱导胃癌MGC-803细胞凋亡的机制

Mechanisms of MVC-induced MGC-803 Cell Apoptosis

摘要: 目的研究N-来酰-L-缬氨酸酯姜黄素(MVC)诱导人胃癌MGC-803细胞凋亡的分子机制。方法采用MTT法检测MVC对肿瘤细胞的生长抑制作用；Hoechst 33342/PI核荧光双染色法检测细胞凋亡的改变；运用Western blot技术检测参与细胞凋亡相关基因的蛋白表达。结果20 μmol/L MVC可明显抑制MGC-803细胞生长，48 h IC50值为12.6 μmol/L；20 μmol/L MVC可诱导MGC-803细胞凋亡；MVC作用后，增加了促凋亡蛋白Bax的表达，抑制了凋亡蛋白Bcl-2 的表达，提高了Caspase-3活性。结论MVC可通过Bcl-2介导的线粒体途径诱导MGC-803 细胞凋亡。

Abstract: ObjectiveTo study on the mechanisms of MVC-induced MGC-803 cell apoptosis. Methods The role of MVC on cell growth was tested by MTT in vitro. Apoptotic cells were detected using Hoechst Hoechst 33342/PI staining. The level of the protein involved in apoptosis metabolism was detected by Western blot. Results MCV markedly inhibidited MGC-803 cell growth and IC50 of the 48 hour was 12.6 μmol/L. Apoptosis was observed with in 48 hour after 20 μmol/L MCV treatment. MCV induced MGC-803 cell apoptosis invloved in the activation of caspase-3,up-regulation of Bax and down-regulation of Bcl-2. ConclusionMCV induced MGC-803 cell apoptosis via activation of Bcl-2.