Journal
INTERNATIONAL IMMUNOPHARMACOLOGY
Volume 33, Issue -, Pages 18-23Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.intimp.2016.01.016
Keywords
MCP-1; Microglia; Activation; Inflammation; ICH
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Funding
- Chongqing Municipal Health Planning Commission [ZY201402096, 2015MSXM059]
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Microglia are activated after intracerebral hemorrhage and induce neuron death by releasing proinflammatory cytokines and chemokines. However, the related mechanism of microglia activation in such conditions remains elusive. MCP-1, the ligand of CCR2 expressed in the central nervous system, could promote microglia proliferation, survival and cytokine secretion. According to the previous findings, we make a hypothesis that whether alternation of MCP-1 level could attenuate microglia activation and toxicity to neuron in intracerebral hemorrhage. To identify that, we interfere with the MCP-1 expression of microglia by RNAi technology, and coculture the microglia and neuron in ICH. The results demonstrated that MCP-1 RNAi inhibited TNF-alpha, IL-1 beta and IL-6 expression in microglia and attenuated neuron injury. In conclusion, the present study suggests that MCP-1 might promote ICH induced microglia activation and toxicity to neuron, and MCP-1 RNAi might provide promising therapeutical strategy for ICH. (C) 2016 Elsevier B.V. All rights reserved.
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