Objective To investigate whether the formyl peptide receptor-1(Fpr1)is involved in microglia-induced inflammatory response after spinal cord injury(SCI)to provide a theoretical basis for reducing neuroinflammatory response after SCI.Methods Thirty adult C57BL/6 male mice were randomly divided into a sham surgery group(sham group)and SCI groups at different time points(1,3,5,7 d after operation),with 6 mice in each group.The expression of Fpr1 protein in the spinal cord was detected by Western blotting at different time points after SCI,and the localization of Fpr1 in microglia was detected by immunofluorescence assay.The time point at which the expression level of Fpr1 protein was highest was selected to create the model for further experiments.The mice were randomly divided into SCI group and Fpr1 inhibitor(HCH6-1)intervention group(HCH6-1 intervention group)with 6 mice in each group,and compared with the sham group.The activation degree of microglia in each group was evaluated by immunofluorescence assay,and the expression of inflammatory factors(interleukin[IL]-1β,IL-18 and tumor necrosis factor-α[TNF-α])and inflammasome(NLRP3,ASC and Caspase-1)proteins in each group were detected by Western blotting.Results Compared with the sham group,Fpr1 expression increased on the first day after SCI,reached its peak on the third day,decreased on the fifth day,and decreased to the same level as the sham group on the seventh day.The results of immunofluorescence staining indicated that Fpr1 was mainly expressed in microglia.Compared with the SCI group,the activation of microglia in the HCH6-1 intervention group was significantly reduced,the expressions of inflammatory factors(IL-1β,IL-18 and TNF-α)and inflammasomes(NLRP3,ASC and Caspase-1)were significantly reduced.Conclusion Fpr1 can mediate the inflammatory response induced by microglia after SCI,and inhibition of Fpr1 may be a new therapeutic strategy to intervene the secondary injury after SCI.
维普
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