Gene silencing of MCP-1 prevents microglial activation and inflammatory injury after intracerebral hemorrhage.

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-α, IL-1β 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.