依托咪酯对子宫内膜癌细胞增殖抑制和凋亡的影响

Effects of etomidate on proliferation inhibition and apoptosis of endometrial cancer cells

目的探究依托咪酯对子宫内膜癌细胞增殖抑制和凋亡的影响。方法实验分为对照组、依托咪酯高剂量组、依托咪酯中剂量组、依托咪酯低剂量组,继续培养细胞48 h进行实验。细胞计数试剂盒8(CCK-8)细胞增殖情况;流式细胞术检测细胞凋亡、细胞周期情况;蛋白质免疫印迹检测细胞中剪切的半胱氨酸天冬氨酸蛋白酶(cleaved Caspase)-3、cleaved Caspase-7、细胞周期依赖性蛋白激酶(CDK)2、CDK4蛋白表达情况。结果与对照组相比,依托咪酯中、高剂量组细胞增殖抑制率、细胞凋亡率、G2-M期细胞百分比,细胞中cleaved Caspase-3、cleaved Caspase-7蛋白表达水平升高(P<0.05),G0-G1期细胞百分比、S期细胞百分比,细胞中CDK2、CDK4蛋白表达水平降低(P<0.05),依托咪酯低剂量组细胞凋亡率,细胞中cleavedCaspase-3、cleavedCaspase-7蛋白表达水平升高(P<0.05),G0-G1期细胞百分比,细胞中CDK2、CDK4蛋白表达水平降低(P<0.05);与依托咪酯低剂量组相比,依托咪酯中、高剂量组细胞增殖抑制率、细胞凋亡率、G2-M期细胞百分比,细胞中cleaved Caspase-3、cleaved Caspase-7蛋白表达水平升高(P<0.05),G0-G1期细胞百分比、S期细胞百分比,细胞中CDK2、CDK4蛋白表达水平降低(P<0.05);与依托咪酯中剂量组相比,依托咪酯高剂量组细胞增殖抑制率、细胞凋亡率、G2-M期细胞百分比,细胞中cleaved Caspase-3、cleaved Caspase-7蛋白表达水平升高(P<0.05),G0-G1期细胞百分比,细胞中CDK4蛋白表达水平降低(P<0.05)。结论依托咪酯能够促进人子宫内膜癌KLE细胞增殖抑制和凋亡,并可诱导其发生G2-M期阻滞。

Objective To explore the effects of etomidate on the proliferation inhibition and apoptosis of endometrial cancer cells. Methods The experiment was divided into control group, etomidate high-dose group, etomidate middle-dose group, etomidate low-dose group, continue to culture the cells for 48 h for the experiment. Cell counting Kit-8(CCK-8) was used to detect cell proliferation;flow cytometry was used to detect cell apoptosis and cell cycle;Western blotting was performed to detect the expression of cleaved Caspase-3, cleaved Caspase-7, cell cycle-dependent protein kinase(CDK) 2, and CDK4 protein in the cells. Results Compared with the control group, the cell proliferation inhibition rate, apoptosis rate, percentage of cells in G2-M phase, and the protein levels of cleaved Caspase-3 and cleaved Caspase-7 in the etomidate(medium and high)-dose groups increased(P<0.05), the percentage of cells in G0-G1 phase, the percentage of cells in S phase, the protein levels of CDK2 and CDK4 in the cells decreased(P<0.05), the apoptotic rate of the etomidate low-dose group, the protein levels of cleaved Caspase-3 and cleaved Caspase-7 in the cells increased(P<0.05), the percentage of cells in G0-G1 phase, the protein levels of CDK2 and CDK4 in the cells decreased(P<0.05);compared with etomidate low-dose group, the cell proliferation inhibition rate, apoptosis rate, percentage of cells in G2-M phase, and the protein levels of cleaved Caspase-3 and cleaved Caspase-7 in the etomidate(medium and high)-dose groups increased(P<0.05), the percentage of cells in G0-G1 phase, the percentage of cells in S phase, the protein levels of CDK2 and CDK4 in the cells decreased(P<0.05);compared with the etomidate middle-dose group, the cell proliferation inhibition rate, apoptosis rate, percentage of cells in G2-M phase,and the protein levels of cleaved Caspase-3 and cleaved Caspase-7 in the etomidate high-dose group increased(P<0.05), the percentage of cells in G0-G1 phase and the protein level of CDK4 in the cells decreased(P<0.05). Conclusion Etomidate can promote the proliferation inhibition and apoptosis of human endometrial carcinoma KLE cells, and induce G2-M phase arrest.