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目的探讨二甲双胍对低氧诱导的大鼠肾上腺嗜铬细胞瘤PC12细胞损伤的影响及其可能的作用机制。方法利用低氧手套箱(0.3%O2)处理PC12细胞,并采用甲紫染色和Annexin-Ⅴ/碘化丙啶(PI)双标法检测细胞生存及凋亡情况;采用CCK8法测定细胞活力;蛋白印迹检测信号通路活化水平及蛋白表达水平。结果低氧(0.3%O2)可对PC12细胞产生时间依赖性的损伤效应;二甲双胍预处理可对低氧造成的PC12细胞损伤产生保护效应,在0.3~1 mmol/L剂量范围内,其保护作用具有剂量依赖性;二甲双胍能激活细胞内腺苷酸活化蛋白激酶(AMP-activated protein kinase,AMPK)信号通路;AMPK激酶选择性抑制剂复合物C预处理细胞后,阻断了二甲双胍对PC12细胞的低氧损伤的保护作用。结论二甲双胍预处理对低氧造成的PC12细胞损伤具有保护作用,AMPK激酶在二甲双胍保护低氧造成的PC12细胞损伤中起着重要作用。
Objective To investigate the effect of metformin on the injury of hypoxic-induced adrenal pheochromocytoma PC12 cells and its possible mechanism. Methods PC12 cells were treated with hypoxia glove box (0.3% O2), cell viability and apoptosis were detected by methylazyl violet staining and Annexin-V / propidium iodide (PI) double staining. Cell viability was measured by CCK8 assay. Western blotting was used to detect the level of activation and protein expression. Results Hypoxia (0.3% O2) had a time-dependent effect on PC12 cells. Pretreatment with metformin had a protective effect on PC12 cells injured by hypoxia, and its protective effect was observed in the dose range of 0.3-1 mmol / L Metformin can activate AMPK (AMPK) signal pathway. After AMPK kinase inhibitor C pretreatment, metformin blocked the proliferation of PC12 cells Hypoxic injury protection. Conclusion Metformin preconditioning protects PC12 cells from hypoxia. AMPK kinase plays an important role in the protection of PC12 cells induced by metformin.