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目的:探讨紫杉醇对肝癌SMMC7721细胞凋亡的诱导作用及对bcl-2和bax基因的影响。方法:用浓度为5μg·ml~(-1)的紫杉醇处理肝癌SMMC7721细胞后,利用DNA琼脂糖凝胶电泳,TUNEL法检测其细胞凋亡;通过原位杂交法、免疫组化法,测定紫杉醇诱导肝癌SMMC7721细胞产生凋亡时,凋亡抑制基因bcl-2和凋亡促进基因bax的mRNA和蛋白表达。结果:紫杉醇作用一定时间后,SMMC7721细胞产生凋亡、bcl-2显著下降、bax表达显著增高。结论:紫杉醇通过调节细胞凋亡抑制基因bcl-2和细胞凋亡促进基因bax的作用,从而诱导肝癌SMMC7721细胞产生凋亡。
Objective: To investigate the induction of paclitaxel on the apoptosis of hepatocellular carcinoma SMMC7721 cells and its effect on bcl-2 and bax genes. Methods: The hepatocellular carcinoma SMMC7721 cells were treated with paclitaxel at a concentration of 5μg · ml ~ (-1), and the apoptosis of SMMC7721 cells was detected by DNA agarose gel electrophoresis and TUNEL method. The in situ hybridization and immunohistochemistry were used to determine the effect of paclitaxel The apoptosis-inducing gene bcl-2 and apoptosis-promoting gene bax mRNA and protein expression were induced when hepatoma SMMC7721 cells were induced to apoptosis. Results: After a certain time of paclitaxel, apoptosis of SMMC7721 cells was induced, bcl-2 was significantly decreased and bax expression was significantly increased. Conclusion: Paclitaxel induces apoptosis in hepatocellular carcinoma SMMC7721 cells through regulating the function of bcl-2 and promoting gene bax.