Methylprednisolone exerts neuroprotective effects by regulating autophagy and apoptosis

• Published in: Neural regeneration research 2016-05, Vol.11 (5), p.823-828
• Main Authors: Gao, Wei, Chen, Shu-rui, Wu, Meng-yao, Gao, Kai, Li, Yuan-long, Wang, Hong-yu, Li, Chen-yuan, Li, Hong
• Format: Article
• Language: English
• Subjects: Analysis; Apoptosis; Autophagy; Autophagy (Cytology); Cell growth; Flow cytometry; Methylprednisolone; Morphology; nerve regeneration; spinal cord injury; methylprednisolone; oxidative stress; N2a cells; autophagy; light chain 3B; Beclin-1; apoptosis; neuroprotection; H 2 O 2; neural regeneration; Oxidative stress; Polyclonal antibodies; Proteins; 氧化损伤; 甲基强的松龙; 相差显微镜; 神经保护作用; 神经元样细胞; 细胞凋亡; 自噬; 蛋白表达
• ISSN: 1673-5374; 1876-7958
• DOI: 10.4103/1673-5374.182711

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 N2 a 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.