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目的探讨姜黄素诱导人胃癌细胞SGC-7901凋亡的可能机制。方法体外培养人胃癌细胞SGC-7901,细胞计数盒8(CCK8)法观察不同浓度姜黄素对胃癌细胞SGC-7901的增殖抑制作用;流式细胞仪检测SGC-7901细胞周期;Western blot检测SGC-7901细胞核转录因子κB(NF-κB)、livin、caspase-3蛋白表达情况。结果与对照组比较,各剂量姜黄素组SGC-7901细胞增殖活力均受到抑制,呈剂量效应关系(r=0.901,P<0.01)与时间效应关系(r=0.389,P<0.01);与对照组(2.8%)比较,20、40、60μmol/L姜黄素组SGC-7901细胞凋亡率[分别为7.7%、13.4%、20.7%]明显升高(P<0.05);与对照组(58.59%)比较,20、40、60μmol/L姜黄素组SGC-7901细胞周期G1期比例[分别为60.24%、65.13%、68.35%]明显升高(P<0.05);与对照组比较,姜黄素组SGC-7901细胞内NF-κB、livin蛋白表达降低,caspase-3蛋白表达升高(P<0.05),呈剂量效应关系。结论姜黄素可抑制人胃癌细胞SGC-7901的活性,其机制可能与姜黄素下调NF-κB信号通路,促进livin解除对caspase的抑制效应而激活caspase-3,发挥其诱导细胞凋亡作用有关。
Objective To investigate the possible mechanism of curcumin-induced apoptosis in human gastric cancer cell line SGC-7901. Methods Human gastric cancer cell line SGC-7901 and CCK8 were used to observe the effects of curcumin on the proliferation of gastric cancer cell line SGC-7901. The cell cycle of SGC-7901 cells was detected by flow cytometry. The expression of SGC- 7901 nuclear factor kappa B (NF-κB), livin, caspase-3 protein expression. Results Compared with the control group, the proliferation activity of SGC-7901 cells in each dose of curcumin was inhibited by dose-effect relationship (r = 0.901, P <0.01) and the time effect (r = 0.389, P <0.01) Compared with control group (58.59), the apoptotic rates of SGC-7901 cells (7.7%, 13.4%, 20.7%, respectively) in 20,40,60μmol / L curcumin group were significantly increased %), The proportion of G1 phase in SGC-7901 cells treated with 20, 40 and 60μmol / L curcumin was significantly higher than that in control group [60.24%, 65.13% and 68.35% respectively] (P <0.05) In SGC-7901 cells, the expression of NF-κB and livin decreased, and the expression of caspase-3 increased (P <0.05), showing a dose-response relationship. CONCLUSION: Curcumin can inhibit the activity of SGC-7901 in human gastric cancer cells, which may be related to the downregulation of NF-κB signaling pathway by curcumin and the activation of caspase-3 by livin to release its inhibitory effect on caspase.