姜黄素通过改变FAK表达和激活caspase诱导人脑胶质瘤U251细胞凋亡

Curcumin induces U251 cell apoptosis via alteration of expression of FAK and activation of caspase

目的研究姜黄素诱导U251细胞凋亡机制。方法20～100μmol·L^-1姜黄素分别处理U251细胞24h后，MTT法测定姜黄素对U251细胞的细胞抑制作用及各种caspase抑制剂对姜黄素作用的影响；通过流式细胞仪检测细胞凋亡；透射电镜观察细胞形态学变化；用免疫细胞化学分析姜黄素对FAK（focal adhesion kinase，粘着斑激酶）蛋白质表达的影响；荧光分光光度法检测caspase-3活性的改变。结果姜黄素明显抑制U251细胞的增殖；诱导U251细胞凋亡；FAK蛋白表达减少；easpase-3活性增强，各种caspase抑制剂可抑制姜黄素诱导的U251细胞凋亡。结论姜黄素通过抑制FAK蛋白的表达和激活caspase途径可诱导U251细胞凋亡。

Aim To study the mechanism of curcumin induced U251 cell apoptosis. Methods U251 cells were treated with 20 - 100μmol · L^-1 curcumin for 24 h and the growth inhibition rates of U251 cells were measured with MTT method. MTT method was used to measure the caspase inhibitors effect on curcumin too. Cell apoptosis was inspected with flow cytometry （FCM） and observed using electron microscope. The protein levels of FAK in U251 cells were observed by SP immunocytochemistry. The activity of caspase-3 was measured by spectrofluorometry. Results Curcumin inhibited the proliferation of U251 cells, induced apop- tosis of U251 cells. At the same time the protein levels of FAK in U251 cells decreased and the activity of caspase-3 increased significantly. The apoptosis of U251 cells was partially reversed by caspase inh）bitors. Conclusion Curcumin induced apoptosis via inhibi- tion of expression of FAK and activation of caspase-3.