Fig 2: LPS Induces microglial-mediated neuroinflammation by Activating CMPK2. (A) Western blot analysis of CMPK2 protein levels under different treatments. (B) Analysis of CMPK2 mRNA expression under different treatments. (C) Immunofluorescence analysis of CMPK2 expression in mouse primary microglial under different treatments. (D) Analysis of morphological differences between treated and control cells. (E) Analysis of the microglial activation marker CD40 expression.F,G. Analysis of mRNA and protein expression levels of IL-6, TNF-α, IL-1β, and TGF-β. The presented data represent the mean ± standard deviation (SD) derived from three independent experiments. Statistical significance of the fold change was determined, with *P < 0.05, **P < 0.01, ***P < 0.001 and ****P < 0.0001 denoting the significance levels.

Fig 3: CMPK2 Induces microglial-mediated neuroinflammation via the cGAS/STING Pathway.A. Western blot analysis of CMPK2 under control plasmid and CMPK2 overexpression plasmid groups.B.Western blot analysis of CMPK2, cGAS, and STING protein levels under different treatments.C. Analysis of CMPK2, cGAS, and STING mRNA expression under different treatments.D. Analysis of morphological differences between treated and control cells.E. Analysis of microglial activation marker CD40 expression.F. Molecular docking analysis of CMPK2 and cGAS interaction.G,H. Analysis of mRNA and protein expression levels of IL-6, TNF-α, IL-1β, and TGF-β. The presented data represent the mean ± standard deviation (SD) derived from three independent experiments. Statistical significance of the fold change was determined, with *P < 0.05, **P < 0.01, ***P < 0.001 and ****P < 0.0001 denoting the significance levels.