Methylprednisolone exerts neuroprotective effects by regulating autophagy and apoptosis  

作　　者：Wei Gao Shu-rui Chen Meng-yao Wu Kai Gao Yuan-long Li Hong-yu Wang Chen-yuan Li Hong Li 

机构地区：[1]Department of Biochemistry, Liaoning Medical University

出　　处：《Neural Regeneration Research》2016年第5期823-828,共6页中国神经再生研究（英文版）

基　　金：supported by the National Natural Science Foundation of China,No.81171799,81471854;the Science and Technology Research Project of Education Department of Liaoning Province of China,No.L2013333;the"College Students’Science and Technology Innovation Project"of Liaoning Medical University Principal Fund-Aohong Boze Fund of China,No.2014D08;the Liaoning Medical University Principal Fund-Aohong Boze Graduate Student Science Research Innovation Fund,No.AH2014017

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 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.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.

关 键 词：nerve regeneration spinal cord injury METHYLPREDNISOLONE oxidative stress N2a cells AUTOPHAGY light chain 3B BECLIN-1 APOPTOSIS NEUROPROTECTION H2O2 neural regeneration 

分 类 号：R651.2[医药卫生—外科学]