阿司匹林增强TRAIL诱导的HepG-2细胞凋亡

目的:研究阿司匹林能否增强肿瘤坏死因子相关凋亡诱导配体(TRAIL)诱导的HepG-2细胞凋亡,并初步探讨其作用机制。方法:HepG-2细胞放入含15%胎牛血清的DMEM培养液中培养,改良苯酚-品红染色观察细胞形态变化,MTT法检测细胞增殖程度,TUNEL法检测细胞凋亡指数,RT-PCR检测细胞中survivinmRNA的表达水平,FCM检测细胞凋亡率和细胞周期。结果:不同浓度的阿司匹林联合TRAIL实验组细胞增殖抑制率明显高于空白对照组及TRAIL和阿司匹林单独用药组,且细胞凋亡指数也明显提高,凋亡率与阿司匹林的浓度呈现剂量依赖关系,联合用药组凋亡相关基因survivin的表达与空白对照组和TRAIL和阿司匹林单用组相比明显下调。结论:阿司匹林能够增强TRAIL诱导的HepG-2细胞凋亡,其作用机制可能与survivin基因的表达下调有关。

Aspirin enhances TRAIL-induced apoptosis in HepG-2 cells

AIM: To investigate the enhancing effect of aspirin on the HepG-2 cell apoptosis induced by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and its underlying mechanism. METHODS: HepG-2 cells were cultured in DMEM medium with 15% fatal bovine serum. Modified carbol fuchsin staining was used to observe the cellular morphology. Cell proliferation was measured by MTT. The method of terminal deoxynucleotide transferase-mediated dUTP nick end labeling (TUNEL) was used to examine the apoptotic index of the cells. RT-PCR was applied to detect survivin gene expression. The apoptotic rate and cell cycle were determined by flow cytometry. RESULTS: Aspirin at different concentrations and TRAIL inhibited the proliferation of HepG-2 cells and the cell apoptotic index was obviously higher than that in control group. Aspirin increased the apoptotic rate in a dose-dependent manner. Aspirin at different concentrations and TRAIL significantly down-regulated the mRNA level of survivin. CONCLUSION: Aspirin enhances the apoptosis of HepG-2 cells induced by TRAIL and the mechanism may be related to down-regulating the mRNA expression of survivin.