尼古丁对L-929细胞凋亡与细胞调控蛋白bcl-2和BAX表达的影响

The L-929 cell apoptosis and bcl-2 and BAX expression caused by nicotine

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 evaluate the expression of bcl-2 and BAX in the L-929 cell apoptosis caused by nicotine. Methods ① The cultured cells stimulated by three concentrations of nicotine（1000μg/ml,10μg/ml,and 0.1μg/ml） were assessed by flow cytometry（FCM） to observe cell apoptosis rate of 48h.②Reversing Transcription-polymerase（RT-PCR） was used to examine the gene expressions of Bcl-2 and Bax after L-929 cell was exposed in 3 concentrations（10μg/ml,1μg/ml,and 0.1μg/ml） for 24h. Results ①Compared with the control groups,the apoptosis of L-929 cell was induced by nicotine,higher rate with increased concentration.②RT-PCR experiments indicated that nicotine exposure enhanced gene expression of Bax,while attenuating the expression of bcl-2. Conclusion Bcl-2 and BAX participate in the L-929 cell apoptosis caused by nicotine.