中国神经再生研究(英文版) ›› 2016, Vol. 11 ›› Issue (5): 823-828.doi: 10.4103/1673-5374.182711

• 原著:神经损伤修复保护与再生 • 上一篇    下一篇

甲基强的松龙调节自噬和凋亡发挥神经保护作用

  

  • 收稿日期:2015-12-22 出版日期:2016-05-20 发布日期:2016-05-20
  • 基金资助:

    国家自然科学基金(81171799,81471854);辽宁省教育厅科学技术研究项目(L2013333);辽宁医学院校长基金-奥鸿博泽基金“大学生科技创新项目”(2014D08);辽宁医学院校长基金—奥鸿博泽研究生科研创新基金资助(AH2014017)

Methylprednisolone exerts neuroprotective effects by regulating autophagy and apoptosis

Wei Gao#, Shu-rui Chen#, Meng-yao Wu, Kai Gao, Yuan-long Li, Hong-yu Wang, Chen-yuan Li, Hong Li*   

  1. Department of Biochemistry, Liaoning Medical University, Jinzhou, Liaoning Province, China
  • Received:2015-12-22 Online:2016-05-20 Published:2016-05-20
  • Contact: Hong Li, M.D., jzmu_lihong@sina.com.
  • Supported by:

    "This research was 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:

有研究表明甲基强的松龙对脊髓继发性损伤后细胞自噬和凋亡有显著的调控作用。实验设想甲基强的松龙可能通过抑制自噬和凋亡来对抗神经细胞的氧化损伤。实验将体外培养的N2a细胞加入10 μM的甲基强的松龙预处理30 min,再加入100 μM H2O2干预24 h。经MTT,倒置相差显微镜观察,流式细胞术及Western blot检测结果发现,甲基强的松龙预处理可保护N2a细胞免受H2O2诱导的氧化损伤,能够维持损伤的N2a细胞形态和数量,显著降低凋亡细胞比例,并下调神经细胞自噬标志性蛋白LC3-B和Beclin-1表达。结果证实,甲基强的松龙通过抑制自噬和凋亡,发挥了来对抗神经细胞氧化损伤的作用。

orcid: 0000-0002-5446-6717(Hong Li)

关键词: 神经再生, 脊髓损伤, 甲基强的松龙, 氧化应激, N2a细胞, 自噬, LC3-B, Beclin-1, 凋亡, 神经保护, H2O2

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."

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