Inhibitory effect of IL-27 on the overactivation of microglia
Neuroinflammation mediated by microglia is essential for the occurrence and development of Alzheimer's disease(AD).Through the analysis of the GEO database,it was found that IL-27 expression decreased in both the cerebral cortex and hippocampus of AD patients.In this study,the AD cell model of BV-2 cells injured by Aβ1-42,the inflammatory cell model of BV-2 cells damaged by LPS,and the inflammatory animal model were established and the effects of IL-27 after its administration in the above models in regulating microglial phenotype and neuroinflammation were evaluated.In the animal models,the number of Iba1+microglia in the hippocampus was detected by immunohistochemistry,the expression of pro-inflammatory factors such as TNF-α,IL-1β and IL-6 was detected by qPCR,ELISA and Western blot,and the expression of M1/M2 phenotypic markers in microglia was detected by qPCR.To further explore the action mechanism of IL-27,Western blot was used to detect the expression levels of NF-κB,p-NF-κB,IκBα and p-IκBα in microglia after administration of IL-27 and Aβ1-42.The results showed that IL-27 alleviated the abnormal activation of microglia induced by lipopolysaccharide(LPS),decreased the expression of pro-inflammatory factors such as TNF-α,IL-1β and IL-6,transformed microglia induced by LPS or Aβ1-42 from neurotoxic M1 to neuroprotective M2,and improved the abnormal phosphorylation of NF-κB and IκBα induced by Aβ1-42.The research suggested that IL-27 can regulate the M1/M2 polarization of microglia induced by Aβ1-42 or LPS,and alleviate neuroinflammation.
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