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Chinese Journal of Clinical Pharmacology and Therapeutics ›› 2015, Vol. 20 ›› Issue (2): 145-150.

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Autophagy activation contributes to the protection of minocycline against oxygen-glucose deprivation and reperfusion in PC12 cells

XIAO Shi-geng1, DONG Wen-bin2, CHENG Min2, YE Xiao-di2, ZHENG Gao-li2   

  1. 1College of Pharmaceutical Science, Zhejiang Chinese Medical University, Hangzhou 310053, Zhejiang, China;
    2Institute of Materia Medica, Zhejiang Academy of Medical sciences, Hangzhou 310013, Zhejiang, China
  • Received:2014-09-12 Revised:2014-12-10 Online:2015-02-26 Published:2015-03-20

Abstract: AIM: To investigate the effects of autophagy on the protection of minocycline in PC12 cells after oxygen-glucose deprivation and reperfusion.METHODS: Cultured PC12 cells were exposed to oxygen-glucose deprivation and then reperfusion, and treated with minocycline (1, 10, 100 μmol/L) or trimethyladenine (3-MA,5 mmol/L) during reperfusion. Cell viability were determined by MTT assay after 6 h of reperfusion. We also stained cells with monodansylcadaverin to observe autophagic vacuole. The expression of protein LC3Ⅱ, Beclin1 and P62/SQSTM l were determined by western blot.RESULTS: Low dose (1, 10 μmol/L) minocycline significantly attenuated cell death cascades after oxygen-glucose deprivation, while the high dose (100 μmol/L) exacerbated the cell injury. The expression levels of LC3Ⅱ and Beclin1 increased more pronouncedly when PC12 cells were treated with minocycline at the higher concentration (1-100 μmol/L). The autophagy inhibitor 3-MA reversed the protection of minocycline by reducing the expression of LC3Ⅱ and Beclin1 and increasing P62/SQSTMl.CONCLUSION: The study suggests that minocycline promotes PC12 cells survival after oxygen-glucose deprivation and reperfusion, which might be mediated by up-regulating LC3Ⅱand Beclin1 expression and inducing autophagy.

Key words: autophagy, minocycline, PC12 cells, oxygen-glucose deprivation

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