左炔诺孕酮诱导体外人子宫肌瘤细胞凋亡的抗肿瘤机制初步研究

目的：探讨左炔诺孕酮诱导体外人子宫肌瘤细胞凋亡的抗肿瘤机制。方法：单层细胞培养后，使用MTT法分析左炔诺孕酮对人子宫肌瘤细胞增殖作用；使用流式细胞术分析左炔诺孕酮对人子宫肌瘤细胞周期与凋亡的影响；使用Western-blot法分析左炔诺孕酮对人子宫肌瘤细胞P53凋亡通路的影响。结果：左炔诺孕酮对人子宫肌瘤细胞的增殖具有明显抑制作用；左炔诺孕酮促使人子宫肌瘤细胞周期阻滞于G₂/M期，并诱导细胞发生凋亡；左炔诺孕酮激活人子宫肌瘤细胞P53凋亡通路而引起细胞发生凋亡。结论：左炔诺孕酮引起人子宫肌瘤细胞周期阻滞于G₂/M期，并使细胞发生凋亡，进而抑制其增殖，这可能与该药物上调P53蛋白的表达，并激活Bcl-2介导的线粒体凋亡途径有关。

Antitumor mechanism in vitro of human uterine leiomyoma cell apoptosis induced by levonorgestrel tablets

OBJECTIVE To study on the antitumor mechanism of human uterine leiomyoma cell apoptosis induced by levonorgestrel tablets in vitro. METHODS After monolayer cell culture, MTT method was used to analyze the proliferation of human uterine leiomyoma cells induced by levonorgestrel tablets. The cell cycle and apoptosis of human uterine leiomyoma cells were analyzed by flow cytometry. Western blot was used to analyze the effect of levonorgestrel tablets on apoptosis pathway about P53 in human uterine leiomyoma cells. RESULTS Proliferation of human uterine leiomyoma cells was inhibited by levonorgestrel tablets. Levonorgestrel tablets induced human uterine leiomyoma cell arrest at G₂/M phase, followed by cell apoptosis. Levonorgestrel tablets activated the apoptosis pathway about P53 in human uterine leiomyoma cells which resulted in cell apoptosis. CONCLUSION Levonorgestrel tablets can cause cell cycle arrest at G₂/M phase and cell apoptosis, and results in cell proliferation inhibition. The effect may be related with increased P53 expression which results in Bcl-2 mediated mitochondrial apoptotic pathway.