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Gao W, Chen SR, Wu MY, et al. Methylprednisolone exerts neuroprotective effects by regulating autophagy and apoptosis. Neural Regen Res. 2016;11(5):823-8doi: 10.4103/1673-5374.182711.
Gao, W., Chen, S. R., Wu, M. Y., Gao, K., Li, Y. L., Wang, H. Y., Li, C. Y., & Li, H. (2016). Methylprednisolone exerts neuroprotective effects by regulating autophagy and apoptosis. Neural regeneration research, 11(5), 823-8. https://doi.org/10.4103/1673-5374.182711
Gao, Wei, et al. "Methylprednisolone exerts neuroprotective effects by regulating autophagy and apoptosis." Neural regeneration research vol. 11,5 (2016): 823-8. doi: https://doi.org/10.4103/1673-5374.182711
Gao W, Chen SR, Wu MY, Gao K, Li YL, Wang HY, Li CY, Li H. Methylprednisolone exerts neuroprotective effects by regulating autophagy and apoptosis. Neural Regen Res. 2016 May;11(5):823-8. doi: 10.4103/1673-5374.182711. PMID: 27335569; PMCID: PMC4904476.
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Neural Regen Res. 2016 May;11(5):823-8. doi: 10.4103/1673-5374.182711.

Methylprednisolone exerts neuroprotective effects by regulating autophagy and apoptosis.

Neural regeneration research

Wei Gao, Shu-Rui Chen, Meng-Yao Wu, Kai Gao, Yuan-Long Li, Hong-Yu Wang, Chen-Yuan Li, Hong Li

Affiliations

  1. Department of Biochemistry, Liaoning Medical University, Jinzhou, Liaoning Province, China.

PMID: 27335569 PMCID: PMC4904476 DOI: 10.4103/1673-5374.182711

Abstract

Methylprednisolone markedly reduces autophagy and apoptosis after secondary spinal cord injury. Here, we investigated whether pretreatment of cells with methylprednisolone would protect neuron-like cells from subsequent oxidative damage via suppression of autophagy and apoptosis. Cultured N2a cells were pretreated with 10 µM methylprednisolone for 30 minutes, then exposed to 100 µM H2O2 for 24 hours. Inverted phase contrast microscope images, MTT assay, flow cytometry and western blot results showed that, compared to cells exposed to 100 µM H2O2 alone, cells pretreated with methylprednisolone had a significantly lower percentage of apoptotic cells, maintained a healthy morphology, and showed downregulation of autophagic protein light chain 3B and Beclin-1 protein expression. These findings indicate that methylprednisolone exerted neuroprotective effects against oxidative damage by suppressing autophagy and apoptosis.

Keywords: Beclin-1; H2O2; N2a cells; apoptosis; autophagy; light chain 3B; methylprednisolone; nerve regeneration; neural regeneration; neuroprotection; oxidative stress; spinal cord injury

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