尾加压素Ⅱ对肺腺癌A549细胞凋亡的影响及相关机制研究

Effect of Urotensin II on the apoptosis of human lung adenocarcinoma A549 cells and the underlying mechanism

目的:探讨尾加压素Ⅱ(U-Ⅱ)对肺腺癌A549细胞凋亡的影响及相关机制。方法:将体外培养A549细胞分为正常对照组、顺铂组(25μg/mL)及U-Ⅱ+顺铂组(10-7mol/L U-Ⅱ+25μg/mL顺铂),TUNEL法测定A549细胞凋亡,免疫细胞化学方法检测A549细胞中Bcl-2和Bax的表达。结果:与正常对照组相比,顺铂组肺腺癌A549细胞的凋亡率明显增加,Bcl-2蛋白表达明显降低,Bax表达明显升高(P<0.01);与顺铂组相比,U-Ⅱ则能够抑制A549细胞的凋亡,上调Bcl-2蛋白表达,下调Bax蛋白表达(P<0.01)。结论:U-Ⅱ可通过上调Bcl-2蛋白表达,下调Bax蛋白表达从而抑制肺腺癌A549细胞凋亡。

AIM：To explore the effect of Urotensin II on the apoptosis of human lung adenocarcinoma A549 cells and its underlying mechnism. METHODS： A549 cells were divided into three groups： Control group, Cisplatin group （25 μg/mL）and Urotensin II＋Cisplatin group（10-7 mol/L U-Ⅱ＋ 25 μg/mL cisplatin）. The effect of Urotensin II on the apoptosis of A549 cells was determined by TUNEL method. The expressions of Bcl-2 and Bax were detected by immunocytochemistry. RESULTS：Comparing with Control group, the apoptotic rate and the expression of Bax were increased, while the expression of Bcl-2 was decreased in Cisplatin group（P0.01）. Urotensin II significantly inhibited Cisplatin-induced apoptosis of A549 cells and antagonized Cisplatin-induced down-regulation of Bcl-2 and up-regulation of Bax（P0.01）. CONCLUSION： Urotensin II inhibits the apoptosis of human lung adenocarcinoma A549 cells by up-regulating the expression of Bcl-2 and down-regulating the expression of Bax.