PPARγ在肾癌细胞凋亡中的调控作用
The Regulatory Effect of PPARy in the Apoptosis against Renal Cell Carcinoma
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摘要: 目的 探讨PPARγ激动剂罗格列酮和抑制剂T0070907对肾癌A498细胞促凋亡, 抗肿瘤的影响.方法 A498细胞分为3组, 分别加入含有PBS, 罗格列酮 (50μmol/L) 以及T0070907 (50μmol/L) 的完全培养液孵育24 h, MTT法检测各组细胞增殖情况, 应用Western Blot和RT-q PCR分析细胞中BAX、Caspase-3、Cyt-C和Bcl-2的表达水平, 分别在光镜和荧光显微镜下观察A498细胞形态变化.结果 MTT实验结果显示, 罗格列酮和T0070907能够明显抑制A498细胞增殖率 (P<0.05) , 上调A498细胞内Caspase-3、Cyt-C及Bax蛋白和m RNA的表达, 下调Bcl-2蛋白和m RNA的表达 (P<0.05) ;经光镜和Hochest染色观察也发现罗格列酮和T0070907能够促进A498细胞凋亡.结论 罗格列酮和T0070907均可抑制肾细胞癌A498细胞的增殖, 诱导其凋亡, 其抗肿瘤机制有可能与PPARγ的介导有关.Abstract: Objective To explore the effects of PPARγ agonist rosiglitazone and inhibitor T0070907 on apoptosis and anti-tumor in renal carcinoma A498 cells.Me thods A498 cells were divided into three groups and PBS, rosiglitazone (50 μmol/L) and T0070907 50 (μmol/L) were added respectively of 24 h incubation completely. each group of cell proliferation was determined by MTT method and Western Blot analysis and RT-q PCR were applied to detect the expression level of BAX, Caspase 3, Cyt C and Bcl-2. A498 cell morphological changes were observed under light microscope and fluorescence microscope. Re s ults MTT experiment results showed that rosiglitazone and T0070907 could significantly inhibit A498 cell proliferation rate (P< 0.05) , increased the protein and m RNA expression levels of Caspase 3, Cyt C and Bax in A498 cell, and decreased the protein and m RNA expression levels of Bcl-2 (P <0.05) ; Microscopic observation and Hochest staining also found that rosiglitazone and T0070907 could promote apoptosis of A498 cells. Conclus ion Rosiglitazone and T0070907 can inhibit the proliferation of renal cell carcinoma A498 cells and induce apoptosis. The anti-tumor mechanism may be related to PPARγ mediation.
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Key words:
- PPARγ /
- T0070907 /
- Rosiglitazone /
- Apoptosis
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