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目的:探讨二甲双胍对甲状腺乳头状癌BCPAP细胞凋亡的影响及其机制。方法:MTT实验分别检测不同浓度(0mmol/L,1mmol/L,5mmol/L,10mmol/L,20mmol/L)二甲双胍和20mmol/L二甲双胍不同时间点(0h,4h,8h,16h,24h,48h)对PTC细胞系BCPAP细胞增殖的影响。流式细胞术检测二甲双胍对细胞凋亡的影响,Western blot检测GRP78、CHOP、Caspase-12蛋白的表达。结果:与0 mmol/L对照组相比,1mmol/L至20mmol/L的二甲双胍可有效降低BCPAP癌细胞的增殖活性(P<0.05);20mmol/L二甲双胍处理BCPAP癌细胞48h后,可呈现明显细胞凋亡,且内质网应激相关蛋白GRP78、CHOP和Caspase-12表达明显增加(P<0.05)。而抑制剂组则可降低BCPAP癌细胞的凋亡率和内质网应激相关蛋白GRP78、CHOP和Caspase-12的表达(P<0.05)。结论:二甲双胍可以通过启动内质网应激有效参与诱导BCPAP细胞凋亡。
Objective: To investigate the effect of metformin on the apoptosis of papillary thyroid carcinoma BCPAP cells and its mechanism. Methods MTT assay was used to detect the effects of metformin at different concentrations (0 mmol / L, 1 mmol / L, 5 mmol / L, 10 mmol / L, 20 mmol / L) and metformin at 20 mmol / L ) On the proliferation of PTC cell line BCPAP cells. Flow cytometry was used to detect the effect of metformin on apoptosis. Western blot was used to detect the expression of GRP78, CHOP and Caspase-12. Results: Compared with 0 mmol / L control group, metformin of 1 mmol / L to 20 mmol / L could effectively reduce the proliferation of BCPAP cancer cells (P <0.05). After treated with 20 mmol / L metformin for 48 hours, (P <0.05). The expressions of GRP78, CHOP and Caspase-12 in endoplasmic reticulum stress were significantly increased (P <0.05). The inhibitor group could reduce the apoptosis rate of BCPAP cancer cells and the expression of endoplasmic reticulum stress related proteins GRP78, CHOP and Caspase-12 (P <0.05). Conclusion: Metformin can effectively participate in inducing BCPAP apoptosis by activating endoplasmic reticulum stress.