Fig. 5

ShRNA PSMC5 treatment shifted microglial polarization from pro-inflammatory phenotypes toward to anti-inflammatory phenotypes after LPS-induced neuroinflammation. A ShRNA PSMC5 decreased the number of TNF-α-positive microglia (M1) and increased the number of YM-1-positive microglia (M2) in the hippocampus. Representative images of triple-staining immunofluorescence for TNF-α (red), YM-1 (green), and IBA-1 (purple) with DAPI nuclear counterstain in the hippocampus. B ShRNA PSMC5 treatment decreased LPS-induced pro-inflammatory cytokines in the serum and brain. Pro-inflammatory cytokines were detected by ELISA and Griess assay. C ShRNA PSMC5 treatment increased LPS-induced anti-inflammatory cytokine production in the serum and brain. Anti-inflammatory cytokines were detected by ELISA. D Effect of shRNA PSMC5 treatment on iNOS and COX-2 levels in the brain after LPS-induced neuroinflammation. ShRNA PSMC5 treatment alleviated the expression of iNOS and COX-2 protein. n = 3–4 mice/group.Data are presented as mean ± SEM. *P < 0.05, **P < 0.01 compared to the control, saline, shRNA PSMC5, and VIPER groups; ^#P < 0.05, ^##P < 0.01 compared to the shRNA PSMC5 + LPS, VIPER + LPS, and shRNA PSMC5 + VIPER + LPS groups, analyzed by one-way ANOVA. Error bars indicate SEM