姜黄素抑制Hedgehog信号诱导胃癌细胞凋亡

目的探讨姜黄素对胃癌细胞MKN45的作用及可能机制。方法不同浓度的姜黄素作用胃癌细胞MKN45后,采用MTT法检测细胞增殖,流式细胞仪检测细胞凋亡,Westernblot技术检测索尼克刺猬信号(Shh)、脑胶质瘤相关癌基因1(GLI1)的表达水平。结果不同浓度的姜黄素与胃癌细胞MKN45共培养后,随着姜黄素浓度的逐渐增加,MKN45细胞的增殖抑制也逐渐增加,经统计学分析发现,姜黄素5μmol/ml组与对照组比较,姜黄素10μmol/ml组与对照组比较,姜黄素20μmol/ml组与10μmol/ml组、5μmol/ml组、对照组比较,差异均有统计学意义(t分别=16.24、14.57、21.16、25.00、38.20,P均<0.05)。胃癌细胞MKN45经姜黄素处理后,姜黄素20μmol/ml组的细胞凋亡率与10μmol/ml组、5μmol/ml组、对照组比较,差异均有统计学意义(t分别=57.05、59.93、61.98,P均<0.05)。经姜黄素处理的MKN45细胞,Shh和GLI1表达均明显降低,与对照组比较,差异均有统计学意义(t分别=3.76、3.55,P均<0.05)。结论姜黄素能通过抑制Hedgehog信号通路,抑制胃癌细胞的增殖,诱导其凋亡。

Curcumin induces apoptosis of gastric cancer cells by inhibiting Hedgehog signaling pathway

Objective To investigate the effects of curcumin on gastric cancer cells and the possible molecular mechanisms. Methods The gastric cancer cells MKN45 were treated with curcumin; growth inhibition ratio of the ceils were measured by MTT assay ;apoptosis were detected by flow cytometery, the expressive level of Shh and GLI1 were detected by western blot. Results Gastric gastric cancer cells MKN45 were cocuitured with different concentration＇s curcumin, the increased growth inhibition rates of the cells were correlated with the increased concentration of curcumin. The growth inhi- bition rates of curcumin （5 μmol/ml ＆ 10μmol/ml） group were significantly different with that of the control group; the growth inhibition rates of curcumin （20μmol/ml） group was significantly different with that of the curcumin （10μmol/ml ＆ 5μmol/ml） group and control group （t=16.24,14.57,21.16,25.00,38.20,P〈0.05）.The apoptosis rates of curcumin （20μmol/ml） group was significantly different with that of the curcumin（ 10μmol/ml ＆ 5 μmol/ml） group and control group（t= 57.05,59.93,61.98,P〈0.05）. The expressive levels of Shh, GLI1 in the curcumin （20 μmol/ml） group were significantly different with that of the control group（t=3.76,3.55,P〈0.05）. Conclusions Curcumin can inhibit proliferation and induce apoptosis of gastric cancer cells by inhibiting Hedgehog signaling pathways.