辣椒素诱导人胃癌MKN-45细胞凋亡及其分子机制的研究

Capsaicin-induced apoptosis in human gastric carcinoma cells MKN-45 and its molecular mechanisms

目的:探讨辣椒素诱导人胃癌MKN-45细胞的凋亡作用及其分子机制。方法:用MTT法检测MKN-45细胞生长情况。荧光光镜、透射电镜、DNA凝胶电泳和流式细胞仪检测细胞凋亡。Westernblot蛋白印迹法检测细胞内Bcl-2、Bax和C-myc蛋白表达。结果:辣椒素对MKN-45细胞有明显的生长抑制及诱导凋亡作用,并呈剂量、时间依赖性。光镜与电镜下可见到明显的凋亡细胞。DNA凝胶电泳显示出特征性凋亡梯状带。蛋白印迹法表明辣椒素可使Bax表达升高,Bcl-2和C-myc表达下降。结论:辣椒素能明显抑制人胃癌MKN-45细胞生长,诱导细胞凋亡,并主要通过调节Bax、Bcl-2和C-myc等蛋白的表达来实现。

Objective To investigate the apoptotic effect of capsaicin on human gastric cancer cells MKN-45 and its molecular mechanisms. Methods MKN-45 cells were treated with capsaicin at various concentrations for different durations. Cell growth was determined by MTT method. Transmission electron microscopy and DNA agarose gel electrophoresis were used to ascertain apoptosis-related alterations in morphology and biochemistry. Flow cytometry was applied to measure the apoptotic rate, so was Western blot to detect the protein expressions of Bcl-2, Bax, and C-myc genes. Results Capsaicin suppressed the growth of MKN-45 cells markedly and induced apoptosis in a dose- and timedependent manner. Under transmission electron microscopy, the treated cells exhibited obvious apoptosis. The characteristic ladder-like DNA fragment appeared in the cells. Western blot assay showed that capsaicin upregulated the Bax expression and downregulated the expressions of Bcl-2 and C-myc. Conclusion Capsaicin can significantly inhibit the growth of MKN-45 cells and induce apoptosis mainly via regulating the expressions of Bax, Bcl-2, and C-myc.