摘要
目的:探讨AMPK(腺苷酸活化蛋白激酶)系统在姜黄素诱导CaOV3人卵巢癌细胞凋亡中的作用及姜黄素对AMPK磷酸化水平及其信号通路的影响。方法:实验分为对照组、姜黄素单独作用组、compound C(AMPK抑制剂)预给药组,SB203580(p38抑制剂)预给药组,AMPK抑制剂单独作用组以及p38抑制剂单独作用组。Western blotting法检测AMPK、p38和p53的磷酸化水平,MTT法检测细胞活力。结果:与对照组相比,姜黄素作用组的AMPK和p38磷酸化水平增加(P<0.05),与姜黄素单独作用组相比,SB203580预处理组的AMPK磷酸化水平下降(P<0.05)。姜黄素作用组的细胞活力低于对照组(P<0.05),compound C和SB203580预处理组的细胞活力高于姜黄素单独作用组(P<0.05)。与对照组相比,姜黄素作用组的p53磷酸化水平(Ser 15)增加(P<0.05),与姜黄素单独作用组相比,compound C(AMPK抑制剂)和SB203580预处理组的p53磷酸化水平(Ser 15)下降(P<0.05)。结论:姜黄素能激活CaOV3细胞的AMPK,而AMPK的激活依赖于p38。AMPK和p38调节p53的磷酸化,并介导姜黄素诱导的细胞凋亡。
Objective： To investigate the effect of AMPK system in CaOV3 ovarian cancer cell apoptosis induced by curcumin and to discuss the underlying transduction pathway. Methods： Cells were randomly divided into six groups： control group, curcumin treated group, Compound C （AMPK inhibitor） pretreatment group, SB203580 （p38 inhibitor） pretreatment group, Compound C treatment group and SB203580 treatment group. The phosphorylation of AMPK, p38 and p53 were detected by Western blotting and cell viability was determined by MTT. Results： Phospho-AMPK and phospho-p38 were higher in curcumin treatment group than those in control group, and phosho-AMPK was lower in SB203580 pretreatment group than that in treatment group. Cell viability was decreased in curcumin treatment group in comparison with control. Compared to curcumin treatment group, cell viability was increased in Compound C pretreatment group and SB203580 pretreatment group. Phospho-p53 was increased in curcumin treatment group in comparison with control. Compared to curcumin treatment group, phosoho-p53 was decreased in Compound C pretreatment group and SB203580 pretreatment group. Conclusions： Curcumin induces AMPK activation in a p38 dependent manner. AMPK and p38 regulate p53 phosphorylation and mediate curcumin inducing cell death in CaOV3 cells.
出处
《现代生物医学进展》
CAS
2009年第4期637-640,657,共5页
Progress in Modern Biomedicine
