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目的探讨尼古丁诱导L-929细胞凋亡及细胞调控蛋白bcl-2和BAX的表达。方法①用不同浓度的尼古丁(1000μg/ml、10μg/ml和0.1μg/ml)作用L-929细胞48h后,采用流式细胞术检测活细胞凋亡率;②不同浓度的尼古丁(10μg/ml、1μg/ml和0.1μg/ml)刺激L-929细胞24h后,逆转录聚合酶链反应(RT-PCR)测定Bcl-2和BAX的活性。结果①与对照组相比,尼古丁实验组诱导L-929细胞凋亡。浓度越大时,则凋亡率越高。②尼古丁与L-929细胞共同作用后,BAX的活性与正常对照组相比表达上调,而Bcl-2的活性表达下降。结论 bcl-2和BAX参与了尼古丁诱导的L-929细胞凋亡。
Objective To investigate nicotine-induced apoptosis of L-929 cells and the expression of cellular regulatory proteins bcl-2 and BAX. Methods ① L-929 cells were treated with different concentrations of nicotine (1000μg / ml, 10μg / ml and 0.1μg / ml) for 48 hours, then the apoptosis rate of live cells was detected by flow cytometry; ② The nicotine , 1μg / ml and 0.1μg / ml) for 24 h. The activities of Bcl-2 and BAX were measured by reverse transcription-polymerase chain reaction (RT-PCR) Results ① Compared with the control group, nicotine experimental group induced the apoptosis of L-929 cells. The higher the concentration, the higher the rate of apoptosis. ② After nicotine combined with L-929 cells, the activity of BAX was up-regulated compared with the normal control group, while the activity of Bcl-2 was decreased. Conclusions bcl-2 and BAX are involved in the nicotine-induced apoptosis of L-929 cells.