本文選題：PPARγ + PTEN�。� 參考：《重慶醫(yī)科大學》2014年碩士論文

【摘要】：目的：探討羅格列酮對人宮頸癌細胞株HeLa細胞體外增殖的影響，以及其可能的機制。 方法：MTT法檢測羅格列酮對Hela細胞增殖的影響；流式細胞技術檢測細胞凋亡率和細胞周期分布的變化；Western-Blot技術檢測羅格列酮干預前后，細胞中PTEN、CyclinD1、磷酸化-Akt（p-Akt）的蛋白水平變化。 結果：MTT結果顯示，羅格列酮能抑制細胞增殖效果明顯,并呈時間和劑量依賴性。流式細胞技術檢測結果顯示，羅格列酮使G1期細胞比例增多，S期細胞比例下降，細胞凋亡率上升至（6.24±1.5）%；WB檢測PTEN蛋白表達上調(diào)、cyclin D1蛋白和磷酸化Akt蛋白表達下調(diào)。 結論：羅格列酮可抑制宮頸癌HeLa細胞增殖、促進細胞凋亡，其機制可能與羅格列酮通過激活PPARγ，誘導PTEN表達、下調(diào)磷酸化Akt（p-Akt）、CyclinD1表達有關。提示羅格列酮有望成為宮頸癌治療藥。
[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 鹵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 緯 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.
【學位授予單位】：重慶醫(yī)科大學
【學位級別】：碩士
【學位授予年份】：2014
【分類號】：R737.33

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