Dong L R, Li M, Li S, Liu A D, Xiong Y J, Tang H, Song X D
Department of Pathology, Affiliated Hospital of North China University of Science and Technology, Tangshan, 063000, China.
Department of Pharmacy, Affiliated Hospital of North China University of Science and Technology.
Lin Chuang Er Bi Yan Hou Tou Jing Wai Ke Za Zhi. 2017 Jun 20;31(12):937-940. doi: 10.13201/j.issn.1001-1781.2017.12.010.
To investigate the role of metformin in inducing apoptosis of papillary thyroid carcinoma BCPAP cells. Using MTT methods to detect effects of metformin on cell proliferation of BCPAP in different concentrations (0 mmol/L, 1 mmol/L, 5 mmol/L, 10 mmol/L, 20 mmol/L) and time course (0 h, 4 h, 8 h, 16 h, 24 h, 48 h). The experiment was divided into four groups: Con, Met, Met+Sal and Met+DM, flow cytometry to detect the rate of apoptosis of BCPAP. Then detect the protein expressions of CHOP, GRP78 and Caspase-12 of 4 groups by Western blot. Compared with the experimental control group, the percentage of cell proliferation index significantly decreased in metformin (0-20 mmol/L and 0-48 h) treatment group. Compared with the experimental control group, the percentage of apoptosis cells significantly increased in metformin treatment group. Compared with the control group, the protein expressions of GRP78, CHOP and Caspase-12 were significantly increased in Met group; While compared with the Met group, the protein expressions of GRP78, CHOP and Caspase-12 were significantly inhibited in the Met+Sal group. Metformin can induced availably BCPAP cell apoptosis by activating endoplasmic reticulum stress mechanism.
探讨二甲双胍诱导甲状腺乳头状癌BCPAP细胞凋亡的作用。采用MTT法检测不同浓度(0 mmol/L、1 mmol/L、5 mmol/L、10 mmol/L、20 mmol/L)和不同时间点(0 h、4 h、8 h、16 h、24 h、48 h)二甲双胍对BCPAP细胞增殖的影响。实验分为四组:对照组、二甲双胍组、二甲双胍+牛磺胆酸钠组和二甲双胍+二十二碳六烯酸组,采用流式细胞术检测BCPAP细胞凋亡率。然后通过蛋白质免疫印迹法检测四组细胞中CHOP、GRP78和Caspase-12的蛋白表达。与实验对照组相比,二甲双胍(0 - 20 mmol/L及0 - 48 h)处理组细胞增殖指数百分比显著降低。与实验对照组相比,二甲双胍处理组凋亡细胞百分比显著增加。与对照组相比,二甲双胍组GRP78、CHOP和Caspase-12蛋白表达显著增加;而与二甲双胍组相比,二甲双胍+牛磺胆酸钠组GRP78、CHOP和Caspase-12蛋白表达显著受到抑制。二甲双胍可通过激活内质网应激机制有效诱导BCPAP细胞凋亡。