Fig. 6.

Liraglutide treatment reduced PGD₂-microglia-provoked neuroinflammation and further neurodegeneration in GPR120 KO mice. GPR120 KO mice were administrated liraglutide (Lira) peripherally for 11 weeks. PGD₂ contents in the hippocampus (A). The protein level determined by western blot analysis (B). The level of H-PGDS (C) and Iba-1 protein (D) in the hippocampus. The immunofluorescence of Iba-1 (E) and Iba-1-positive cell counts in the CA3 (F) and hippocampus (G). Scale bar = 50 μm. The level of DCX protein in the hippocampus (H). The immunofluorescence of DCX (I) and DCX-positive cell counts in the dentate gyrus (J). Scale bar = 80 μm. The level of SOD2 mRNA (K) and protein (L) expression. Data are presented as the mean ± SEM, n = 5 per group. Statistical analysis was performed using a student’s t test (*p < 0.05; **p < 0.01 vs. GPR120 KO + Sham). Hippocampal volume of WT and GPR120 KO mice, and Liraglutide-treated GPR120 KO mice (M). Statistical analysis was performed using one-way ANOVA followed by Newman–Keuls post-hoc test (***p < 0.001 vs. WT, ^#p < 0.05 vs. GPR120 KO + Sham). The level of synaptophysin (Syn) (N) and PSD95 (O) protein in the hippocampus. Learning and memory performance were evaluated using the Y-maze (P). Data are presented as the mean ± SEM, n = 5 per group. Statistical analysis was performed using a student’s t test (*p < 0.05 vs. GPR120 KO + Sham). Morris water maze test: Escape latency (Q) and Time platform crossed (R). Data are mean ± SEM, n = 10 per group. Statistical analysis was performed using two-way ANOVA followed by post-hoc Tukey test (*p < 0.01; ***p < 0.001 vs. WT)