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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。
AIM: To investigate the role of AMPK (adenylate activated protein kinase) system in curcumin-induced apoptosis in human ovarian cancer cell line CaOV3 and the effect of curcumin on AMPK phosphorylation and its signaling pathway. Methods: The experiment was divided into control group, curcumin alone group, compound C (AMPK inhibitor) pretreatment group, SB203580 (p38 inhibitor) pretreatment group, AMPK inhibitor alone group and p38 inhibitor alone group . The phosphorylation levels of AMPK, p38 and p53 were detected by Western blotting. The viability of cells was detected by MTT assay. Results: Compared with the control group, the levels of AMPK and p38 phosphorylation were increased in the curcumin group (P <0.05). Compared with the curcumin group, the AMPK phosphorylation level in the SB203580 pretreatment group decreased (P <0.05) . The cell viability of curcumin group was lower than that of control group (P <0.05). The cell viability of compound C and SB203580 pretreatment group was higher than curcumin group (P <0.05). Compared with the control group, the level of p53 (Ser 15) increased (P <0.05) in the curcumin-treated group. Compared with the curcumin-treated group, the levels of p53 phosphorylation of the compound C (AMPK inhibitor) and SB203580 (Ser 15) decreased (P <0.05). Conclusion: Curcumin can activate AMPK in CaOV3 cells, whereas the activation of AMPK depends on p38. AMPK and p38 regulate p53 phosphorylation and mediate curcumin-induced apoptosis.