罗格列酮对人宫颈癌HeLa细胞增殖及机制的研究

发布时间：2018-06-19 10:57

本文选题：PPARγ + PTEN　；参考：《重庆医科大学》2014年硕士论文

【摘要】：目的：探讨罗格列酮对人宫颈癌细胞株HeLa细胞体外增殖的影响，以及其可能的机制。方法：MTT法检测罗格列酮对Hela细胞增殖的影响；流式细胞技术检测细胞凋亡率和细胞周期分布的变化；Western-Blot技术检测罗格列酮干预前后，细胞中PTEN、CyclinD1、磷酸化-Akt（p-Akt）的蛋白水平变化。结果：MTT结果显示，罗格列酮能抑制细胞增殖效果明显,并呈时间和剂量依赖性。流式细胞技术检测结果显示，罗格列酮使G1期细胞比例增多，S期细胞比例下降，细胞凋亡率上升至（6.24±1.5）%；WB检测PTEN蛋白表达上调、cyclin D1蛋白和磷酸化Akt蛋白表达下调。结论：罗格列酮可抑制宫颈癌HeLa细胞增殖、促进细胞凋亡，其机制可能与罗格列酮通过激活PPARγ，诱导PTEN表达、下调磷酸化Akt（p-Akt）、CyclinD1表达有关。提示罗格列酮有望成为宫颈癌治疗药。
[Abstract]:Aim: to investigate the effect of rosiglitazone on the proliferation of human cervical cancer cell line HeLa in vitro and its possible mechanism. Methods the effects of rosiglitazone on the proliferation of Hela cells were detected by cell line MTT assay and the changes of cell apoptosis rate and cell cycle distribution by flow cytometry. Western Blot was used to detect the changes of protein levels of PTEN- cyclin D1 and phosphorylated-Aktt- Akt1 before and after rosiglitazone treatment. Results the cell proliferation was inhibited by rosiglitazone in a time and dose-dependent manner. The results of flow cytometry showed that rosiglitazone increased the proportion of G1 phase cells and decreased the proportion of S phase cells, and the apoptosis rate increased to 6.24 卤1.5%. The expression of PTEN protein up-regulated the expression of cyclin D1 protein and phosphorylated Akt protein. Conclusion: rosiglitazone can inhibit the proliferation of cervical cancer HeLa cells and promote apoptosis. The mechanism of rosiglitazone may be that rosiglitazone induces the expression of PTEN by activating PPAR 纬 and down-regulating the expression of phosphorylated Akttnp-Aktnin D1. The results suggest that rosiglitazone is expected to be a therapeutic drug for cervical cancer.
【学位授予单位】：重庆医科大学
【学位级别】：硕士
【学位授予年份】：2014
【分类号】：R737.33

【参考文献】