Objective To explore the effect of hepatocyte growth factor(HGF)on microglia-mediated neuroinflammation and its regulatory mechanism,and to provide experimental basis and theoretical reference for the determination of possible treatment targets.Methods The mouse immortalized cell line-BV2 cells,which retain multiple morphological and functional characteristics of microglia,were divided into a control group and a HGF group.The effects of HGF on the activity of NF-κB signaling pathway and subsequent expression of neuroinflammatory factors were determined by tyrosine phosphorylated proteomic analysis,cell survival assay,quantitative real time polymerase chain reaction(qRT-PCR)and western blot(WB).Results Tyrosine phosphorylated proteomic analysis showed that after addition of HGF,NF-κB signaling was one of the most enriched pathways in BV2 cells.At 1 hour after the addition of HGF with different concentrations,the proliferation activity of BV2 cells was decreased.At both 6 hours and 12 hours after the supplementation of HGF with various concentrations,the proliferation activity of BV2 cells increased at early stage,while decreased at late stage.qRT-PCR found that HGF could upregulate the transcription level of inflammatory factors derived from BV2 cells(iNOS,TNF-α,IL-1β).WB also showed that HGF could promote protein translation of associated inflammatory factors(TNF-α,NF-κB p65).Conclusions This study confirms the role of HGF in promoting neuroinflammation by activating the NF-κB signaling pathway in BV2 cells and its mechanism.It provides important clues to further explore the regulatory strategies on neuroinflammation to develop more effective treatment in the clinic.
维普
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