维生素B12对氧化应激损伤下神经细胞的保护机制

doi:10.3969/j.issn.2095-9400.2020.06.004

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Abstract Objective: To explore the protective effect of Vitamin B12 pretreatment on PC12 cell injury induced by hydrogen peroxide and of its influence on autophagy and apoptotic protein expression. Methods: PC12 cells were divided as the control group (Control) with RPMI 1640 culturethe injury group (H2O2) with RPMI 1640 culture plus 200 μmol/L hydrogen peroxide stimulation and the Vitamin B12 protection group (H2O2+Vit B12) with RPMI 1640 culture plus 200 μmol/L vitamin B12 and 200 μmol/L hydrogen peroxide stimulation. Cell growth was examined 24 h later, and apoptosis and autophagy-related protein expression were detected by Western blot. Results: Compared with the Control group, the cell survival rate, the level of cell DNA replication, the expression level of Bcl-2 and P62 protein, the expression level of Bax, ATG-5 and LC3 protein, and the activation number of LC3 in cytoplasm increased significantly in the injury group (all P<0.05). Compared with the injury group, the cell survival rate and the level of cell DNA replication in the vitamin B12 protected group increased, the expression level of Bcl-2 and P62 protein increased, the expression level of Bax, ATG-5 and LC3 protein significantly decreased, and the activation number of LC3 in the cytoplasm decreased (all P<0.05). Conclusion: Vitamin B12 can inhibit oxidative stress-induced apoptosis by regulating autophagy.

Key words： vitamin B12 oxidative stress nerve cell autophagy

Received: 03 November 2019

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https://xb.wmu.edu.cn/EN/10.3969/j.issn.2095-9400.2020.06.004 OR https://xb.wmu.edu.cn/EN/Y2020/V50/I6/449

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