Fig. 5

CAC extract inhibited macrophage-mediated inflammation response via PI3K-Akt pathway. A LPS (1 μg/ml) with or without CAC (50, 100 and 200 μg/ml) did not affect cell viability. B CAC extract attenuated NO production. C–E CAC extract decreased mRNA expression levels of IL-6 (B), iNOS (C) and MCP-1 (D). F CAC extract inhibited PI3K-Akt-mTOR pathway in LPS-activated RAW264.7 cells. G Quantitative analysis for relative phosphorylation levels of PI3K (p-PI3K), Akt (p-Akt) and mTOR (p-mTOR) were performed by normalizing to model group. *P < 0.01 vs. LPS group; **P < 0.01 vs. LPS group; ***P < 0.001 vs. LPS group; ^## P < 0.001 vs. control group; ^### P < 0.001 vs. control group; N.S., not significant by ANOVA with Dunnett’s post-hoc test