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

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...

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Published in:BioMed research international 2016-01, Vol.2016 (2016), p.1-14
Main Authors: Yao, Tianchen, Wan, Zhanghui, Li, Haihong, Mei, Xifan, Gao, Wei, Liu, Zhiyuan, Wang, Hongyu, Li, Chenyuan, Bi, Jing, Han, Donghe, Wang, Guannan, Li, Dingding, Gao, Kai
Format: Article
Language:English
Subjects:
Analysis
Animals
Apoptosis
Autophagy
Autophagy - drug effects
Biochemistry
Biomedical research
Bone surgery
Cell death
Cells, Cultured
Cytokines
Cytokines - metabolism
Heart attacks
Inflammation
Investigations
Male
Medical research
Methylprednisolone
Methylprednisolone - pharmacology
Microglia - drug effects
Models, Biological
Neuroprotective Agents - pharmacology
Neurosciences
Political aspects
Proteins
Rats
Rats, Sprague-Dawley
Rodents
Spinal Cord - chemistry
Spinal Cord - drug effects
Spinal Cord - metabolism
Spinal cord injuries
Spinal Cord Injuries - metabolism
Spinal Cord Injuries - pathology
Studies
Tumor necrosis factor-TNF
Zinc - analysis
Zinc - metabolism
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Summary: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.
ISSN:2314-6133
2314-6141
DOI:10.1155/2016/6090316