Methylprednisolone exerts neuroprotective effects by regulating autophagy and apoptosis

Neural Regeneration Research

关键词: nerve regeneration;    spinal cord injury;    methylprednisolone;    oxidative stress;    N2a cells;    autophagy;    light chain 3B;    Beclin-1;    apoptosis;    neuroprotection;    H 2 O 2;    neural regeneration;   

DOI  :  10.4103/1673-5374.182711

来源: DOAJ

【 摘 要 】

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 H 2 O 2 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 H 2 O 2 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.

【 授权许可】

Unknown