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目的探讨二甲双胍对听神经细胞株HEI-OC1放射性损伤的保护作用及可能的分子机制。方法体外培养听神经细胞株HEI-OC1,实验分为正常对照组、照射组、照射+二甲双胍干预组(干预组),MTT法检测各组细胞的生长曲线,流式细胞术检测各组细胞的凋亡率,超氧化物歧化酶(SOD)和丙二醛(MDA)检测试剂盒检测氧化应激指标的改变,免疫印迹检测凋亡相关蛋白Bax及Bcl-2的表达。结果照射后HEI-OC1细胞的生长受到抑制,不同浓度的二甲双胍干预能够减轻照射导致的细胞生长抑制。正常对照组、照射组及干预组细胞凋亡百分比分别为(2.58±0.21)%、(8.92±0.19)%、(3.69±0.18)%,提示二甲双胍干预后显著减少了照射引起的细胞凋亡,且凋亡因子Bax和Bcl-2的蛋白表达也较照射组明显降低(P<0.05)。与正常对照组相比,照射组SOD活性下降[(0.82±0.08)U/mg vs(2.36±0.12)U/mg],MDA含量增加[(1.36±0.15)nmol/mg vs(0.61±0.09)nmol/mg],而采用二甲双胍干预后,SOD活性上升(1.91±0.13)U/mg,MDA含量有所下降(0.78±0.10)nmol/mg,差异均有统计学意义(P<0.05)。结论二甲双胍能够减轻射线对听神经细胞的放射性损伤,该损伤机制与二甲双胍对氧化应激反应的抑制有关。
Objective To investigate the protective effect of metformin on radiation injury of auditory nerve cell line HEI-OC1 and its possible molecular mechanism. Methods Cultured auditory neuronal cell line HEI-OC1 was divided into normal control group, irradiation group and irradiation + metformin intervention group (intervention group). The growth curve of each group was detected by MTT method. The apoptosis of each group was detected by flow cytometry (SOD) and malondialdehyde (MDA) were measured to detect the changes of oxidative stress. Western blotting was used to detect the expression of Bax and Bcl-2. Results The growth of HEI-OC1 cells was inhibited after irradiation. Different concentrations of metformin could reduce the cell growth inhibition induced by irradiation. The percentage of apoptotic cells in normal control group, irradiation group and intervention group were (2.58 ± 0.21)% and (8.92 ± 0.19)%, (3.69 ± 0.18)%, respectively, which suggested that metformin significantly reduced apoptosis after irradiation, The protein expressions of Bax and Bcl-2 were also significantly decreased (P <0.05). Compared with the normal control group, the SOD activity decreased ([(0.82 ± 0.08) U / mg vs (2.36 ± 0.12) U / mg] in the irradiation group and MDA content increased by 1.36 ± 0.15 nmol / mg vs 0.61 ± 0.09 (1.91 ± 0.13) U / mg and MDA content decreased (0.78 ± 0.10) nmol / mg, respectively, with statistical significance (P <0.05) after treatment with metformin. Conclusion Metformin can reduce the radioactive injury of auditory nerve cells by radiation, which is related to the inhibition of metformin on oxidative stress.