D-24851衍生物YB-N12诱导Hela细胞凋亡及其机制

目的:研究D-24851衍生物YB-N12能否诱导宫颈癌细胞株(Hela细胞)发生凋亡及其作用机制。方法:对数生长细胞培养于24孔培养板内24h,给药组加入不同浓度的YB-N12,对照组加入与给药组等体积的DMSO的培养液,培养24h后检测细胞凋亡数。采用MTT、荧光显微镜检测凋亡细胞、DNA ladder方法进行凋亡检测,用RT-PCR方法检测凋亡过程中相关基因表达的变化。结果:D-24851衍生物YB-N12在体外试验中对Hela细胞的杀伤力强,荧光显微镜观察到了凋亡小体,DNA ladder法检测到凋亡时DNA降解形成的梯带。在凋亡过程中,凋亡相关基因p53表达明显增加(P<0.05),而bcl-2表达下降(P<0.05)。结论:D-24851衍生物YB-N12能诱导Hela细胞发生凋亡,其机制可能与p53基因表达上调及bcl-2基因表达下调有关。

Study on Mechanism of D-24851(YB-N12)Induced Apoptosis in Hela Cells

Objective:To study whether the derivate of D-24851(YB-N12) can induce apoptosis in Hela cell lines and its possible mechanisms of apoptosis. Methods: Morphological changes of YB-N12 were tested in MTT assay. Expressions of p53 mRNA,bcl-2 mRNA in Hela cells exposed to YB-N12 were investigated by RT-PCR. Results: The results of MTT assay showed the potent cytotoxic effect on human galactophore cancer. After treatment of Hela cells with YB-N12,apparent morphological changes were found by Hoechest staining. YB-N12 evoked typical apoptotic features such as membrane blebbing,cell shrinkage and detachment,and nuclear condensation. The promoted expression of p53 protein and innvbited expression of bcl-2 by YB-N12 were detected using RT-PCR( P < 0.05 ). Conclusion: YB-N12 induces apoptosis of Hela cells in vitro by promoting p53 and inhibiting bcl-2 expressions in a dose-dependent manner.