二甲双胍对大鼠催乳素瘤MMQ细胞增殖和凋亡的影响及机制

发布时间：2018-05-31 10:58

本文选题：催乳素瘤 + 二甲双胍　；参考：《重庆医科大学》2017年硕士论文

【摘要】：目的:探讨二甲双胍对大鼠催乳素瘤MMQ细胞增殖、周期和凋亡的影响及其机制。方法:采用(1.25、2.5、5、10、20)mmol/L二甲双胍处理MMQ细胞48 h,CCK-8法检测细胞增殖能力,流式细胞术检测细胞周期及细胞凋亡,Western blot法检测AMP活化的蛋白激酶(AMPK)、磷酸化的AMPK(p-AMPK)、哺乳动物雷帕霉素靶蛋白(m TOR)、磷酸化的m TOR(p-m TOR)、胰岛素样生长因子1受体(IGF-1R)、胞外信号调节激酶1/2(ERK1/2)、磷酸化的ERK1/2(p-ERK1/2)、蛋白激酶B(PKB/AKT)、磷酸化的AKT(p-AKT)、P21、细胞周期蛋白依赖激酶4(CDK4)、细胞周期蛋白D1(cyclin D1)、胱天蛋白酶3(caspase-3)、裂解的caspase-3(c-caspase-3)、B淋巴细胞瘤-2(Bcl-2)、Bcl-2相关X蛋白(BAX)的变化。结果:二甲双胍处理后,抑制MMQ细胞增殖,使细胞周期阻滞在G0/G1期,诱导细胞凋亡;周期相关蛋白P21增加,CDK4、cyclin D1水平降低;凋亡相关蛋白c-caspase-3增加,caspase-3、Bcl-2降低;p-AMPK水平增加、p-m TOR水平降低;IGF-1R、p-AKT及p-ERK水平降低。结论:二甲双胍能抑制MMQ细胞增殖,诱导MMQ细胞周期阻滞在G0/G1期,诱导MMQ细胞凋亡;二甲双胍作用机制可能包含激活AMPK/m TOR通路以及抑制IGF-1R通路。
[Abstract]:Aim: to investigate the effect of metformin on proliferation, cycle and apoptosis of prolactin tumor MMQ cells and its mechanism. Methods: the proliferation ability of MMQ cells was measured by CCK-8 method after treated with metformin for 48 h. Detection of cell cycle and apoptosis by flow cytometry Western blot assay for AMP activated protein kinase, phosphorylated AMPK, mammalian rapamycin target protein mTORA, phosphorylated m TOR(p-m torus, insulin-like growth factor-1 receptor IGF-1RN, extracellular faith 1 / 2 / 2 ERK1 / 2, phosphorylated ERK1 / 2 p-ERK1 / 2, protein kinase BK / PKB / AKT, phosphorylated AKTP-AKT1, cyclin dependent kinase 4, CDK4, cyclin D1(cyclin D1, cystein3caspase-3, cleavage of caspase-3, caspase-3caspase-3, caspase-3, c-caspase-3, Bcl-2, Bcl-2Bcl-2Bcl-2p2Bcl-2Bcl-2BX-1, cyclin D _ 1, cystatin D _ 1, cystatin 3caspase-3, cleavage of caspase-3, c-caspase-3, Bcl-2. Results: metformin inhibited the proliferation of MMQ cells, blocked the cell cycle in G0/G1 phase and induced apoptosis, and P21 increased the level of cyclin D1. Apoptosis-related protein c-caspase-3 increased the level of caspase-3 Bcl-2 decreased the level of p-AMPK increased the level of p-m TOR decreased the level of IGF-1Rnp-AKT and p-ERK. Conclusion: metformin can inhibit the proliferation of MMQ cells, induce MMQ cell cycle arrest in G0/G1 phase and induce MMQ cell apoptosis, and the mechanism of metformin may involve the activation of AMPK/m TOR pathway and the inhibition of IGF-1R pathway.
【学位授予单位】：重庆医科大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R736

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