Table of Contents Author Guidelines Submit a Manuscript
BioMed Research International
Volume 2016, Article ID 6090316, 14 pages
Research Article

MP Resulting in Autophagic Cell Death of Microglia through Zinc Changes against Spinal Cord Injury

1Department of Orthopedic Surgery, First Affiliated Hospital of Liaoning Medical University, Jinzhou 121000, China
2Department of Chemistry, College of Pharmacy, Liaoning Medical University, Jinzhou 121000, China
3Department of Neurobiology , Key Laboratory of Neurodegenerative Diseases of Liaoning Province, Liaoning Medical University, Jinzhou 121000, China
4Department of Basic Medical Sciences, Liaoning Medical University, Jinzhou 121000, China

Received 4 February 2015; Accepted 16 February 2015

Academic Editor: Xuanjun Zhang

Copyright © 2016 Dingding Li et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Methylprednisolone pulse therapy (MPPT), as a public recognized therapy of spinal cord injury (SCI), is doubted recently, and the exact mechanism of MP on SCI is unclear. This study sought to investigate the exact effect of MP on SCI. We examined the effect of MP in a model of SCI in vivo and an LPS induced model in vitro. We found that administration of MP produced an increase in the Basso, Beattie, and Bresnahan scores and motor neurons counts of injured rats. Besides the number of activated microglia was apparently reduced by MP in vivo, and Beclin-1 dependent autophagic cell death of microglia was induced by MP in LPS induced model. At the same time, MP increases cellular zinc concentration and level of ZIP8, and TPEN could revert effect of MP on autophagic cell death of microglia. Finally, we have found that MP could inhibit NF-κβ in LPS induced model. These results show that the MP could result in autophagic cell death of microglia, which mainly depends on increasing cellular labile zinc, and may be associated with inhibition of NF-κβ, and that MP can produce neuroprotective effect in SCI.