白杨素对人胃癌SGC-7901细胞增殖与凋亡的影响

Chrysin Inhibiting Proliferation and Inducing Apoptosis in Gastric Cancer SGC-7901 Cells

目的探讨白杨素(Chrysin,ChR)诱导人胃癌SGC-7901细胞株凋亡的作用及机制。方法分别用10、20、40、80μM的ChR处理人胃癌细胞株SGC-790148h,采用MTT比色法检测ChR对SGC-7901细胞的增殖抑制效应;采用丫啶橙(AO)染色、流式细胞术检测ChR诱导SGC-7901细胞凋亡的发生;应用Western-blot法检测凋亡相关基因NF-κB、Bcl-2、Bax的蛋白表达,并用计算机图像分析软件进行半定量分析。结果MTT比色法显示的10～80μM的ChR在体外对人胃癌SGC-7901细胞有增殖抑制率为:9.71%～53.64%,该作用呈浓度依赖性;AO染色荧光显微镜观察ChR在体外能诱导人胃癌SGC-7901细胞发生凋亡,出现早期凋亡细胞及凋亡小体;流式细胞术检测结果显示:ChR呈浓度依赖性地诱导SGC-7901细胞凋亡,凋亡率为2.35%～20.8%;Western-blot检测结果显示:凋亡相关基因Bcl-2、NF-κB蛋白表达下调,Bax蛋白表达上调。结论ChR对体外培养人胃癌细胞具有增殖抑制和诱导凋亡作用,呈浓度依赖性。ChR对人胃癌细胞增殖抑制和诱导凋亡作用机制可能与其抑制NF-κB活化、下调Bcl-2蛋白表达和上调Bax蛋白表达相关。

Objective To study the anticancer function and possible mechanism of Chrysin on gastric cancer cells（SGC-7901）. Methods The cells of human gastric cancer cell line SCR2-7901 was treated respectively with Chrysin at different concentration 10,20,40,80μM for 48h The proliferation inhibitory rate was measured by MTT assay. Acridine orange （AO）staining and flow cytometry （FCM） were used to detect apoptosis. Western blot assay was used to detect the expression of apoptosis related genes NF-κB, Bcl-2,Bax. The semi-quantification of protein expression was analyzed by computer-image-analysis. Resuits When compared with control group, the proliferation could be inhibited by ChR in concentration of 10-80μM, with inhibitory ratios being 9. 71 -53.64% （P〈0.05）. The effect increased with concentration. Partial SGC-7901 cells presented characteristic morphological changes of apoptosis which was detected by acridine orange staining. ChR could induce SGC-7901 cells lines apoptosis in dose-dependent manner, The apoptosis rate was 2. 35%-20. 8% which was detected by FCM. The protein levels of NF- κB, Bcl-2 were down-regulated, while those of Bax up-regulated. Conclusion ChR could restrain the proliferation and induce apoptosis of SCA2-7901 in a dose-dependent manner. Inhibition of growth and induction of apoptosis of SGC-7901 cells by ChR is associated with down-regulation of NF-κB and Bcl-2 protein level and up-regulation of Bax protein expression.