4-HPR体外诱导A549细胞凋亡与Bax/Bak蛋白相关性研究

4-HPR effects on apoptosis of A549 in vitro through changing Bax/Bak protein expression

目的:观察4-HPR对肺腺癌细胞A549凋亡的影响并探讨其机制。方法:不同剂量4-HPR处理A549细胞,倒置显微镜观察A549细胞形态学变化和对细胞生长的抑制作用,Hoechst33258染色观察凋亡情况,Western Blot分析凋亡相关蛋白Bax/Bak等的表达。结果:细胞数目随药物浓度增加而减少,失去正常生长,光泽度下降,变小变圆;细胞凋亡程度随药物浓度增加而增强,细胞核肿胀变圆,致密浓染或碎裂;凋亡过程,Bax/Bak、P53表达明显增加。结论:4-HPR可明显抑制肺腺癌A549细胞的增殖,增加Bax/Bak、P53的表达,促进A549凋亡,为进一步探讨4-HPR治疗肺腺癌的机制提供实验依据。

Objective：To observe the effects of N-（4-Hydroxyphenyl）retinamide（4-HPR）induced apoptosis in vitro in A549,a human alveolar adenocarcinoma cell line,and its inducing mechanisms in the cells.Methods： A549 cells were treated with different concentrations of 4-HPR for observation of the cellular morphology and inhibitory effects by inverted microscope and detection of the apoptosis by Hoechst 33258 staining through a fluorescent microscope.Western blot was used to examine the expression of the proteins associated with apoptosis Bax/Bak.Results： Increased concentration of 4-HPR treatment resulted in the cell decrease,loss of normal growth,blurred glossiness and small and round configuration,and yet enhanced degree of apoptosis which was grossly seen swollen and round nuclei,densified staining or fragmentation.4-HPR treatment also led to a significant increase in Bax/Bak and P53 levels.Conclusion： 4-HPR can significantly inhibit the proliferation and induce apoptosis of A549 cells through protein Bax/Bak and P53 expression enhancement,which may lay the foundation for the laboratory work for further investigation of 4-HPR mechanisms associated with the therapy of pulmonary adenocarcinoma.