紫杉醇诱导HL-60细胞凋亡对Bcl-2基因家族的影响

Effect of paclitaxel-induced apoptosis on HL-60 cells on Bcl-2 gene family

目的研究Bcl-2基因家族在紫杉醇诱导HL-60细胞凋亡中的表达水平变化。方法DNA凝胶电泳法检测细胞凋亡;RT-PCR法检测在紫杉醇诱导前后Bcl-2基因家族的表达水平。结果紫杉醇诱导HL-60细胞凋亡具有剂量依赖性,结果支持紫杉醇诱导HL-60细胞凋亡有剂量依赖性的观点,同时也观察到了低剂量紫杉醇(10-8)即可诱导Bad基因表达明显增加,高剂量紫杉醇(10-6)才可诱导Bcl-2基因表达明显减弱,但未见Bax基因和Bcl-xl基因表达的明显变化。结论紫杉醇能通过诱导细胞凋亡杀伤HL-60细胞,而此凋亡可能与Bad的表达上调和Bcl-2基因表达下调有关,而与Bax和Bcl-xl的表达无关。

[ Objective ] To study the changes of Bcl-2 gene family expression levels in the process of paclitaxel- induced apoptosis on HL-60 cells. [Methods] DNA gel electrophoresis was used to demonstrate DNA fragmentations. Reverse transcriptase polymerase chain reaction （RT-PCR） was used to detect Bcl-2 expression levels. [ Resuits ] Paclitaxel-induced apoptosis on HL-60 cells has a dose-dependent quality. Meanwhile, according to the RTPCR results, we have observed that the low dose of paclitaxel （10~） could induce the increasing of the Bad gene expressions obviously. While, the high dose of paclitaxel （10-6） could obviously induce the decreasing of the Bel-2 gene expressions. But we haven＇t observed the obvious changes of expressions of Bax gene and Bcl-xl gene. [ Conclusions ] Paclitaxel could kill the HL-60 cells by inducing apoptosis. And it were possibly related with Bad upregulation expression and Bcl-2 downregulate expression, and irrelevant with Bax expression level and Bcl-xl expression level.