Figure 1

MSP alleviates PA-induced inflammation in primary mouse hepatocytes. (a) Representative western blotting analysis (left) and quantification of the fold change relative to the vehicle control (right) of RON, AMPK and ACC phosphorylation upon MSP treatment for the indicated amount of time. Data are expressed as the mean±s.e.m. (n=6). *P<0.05 vs Ctl. (b) Representative western blot (top) and quantification of the fold change relative to the vehicle control (bottom) of AMPK and ACC phosphorylation for the indicated treatments. Data are expressed as the mean±s.e.m. (n=6). *P<0.05 vs Ctl; ^#P<0.05 vs PA. (c–e) Real-time quantitative PCR analysis of genes involved in inflammation (c), lipogenesis (d) and fatty acid oxidation (e) from the hepatocytes treated as indicated. Each value indicates the amount of mRNA relative to the vehicle control-treated hepatocytes. Cyclophilin A was used as the invariant control. Data are expressed as the mean±s.e.m. (n=6). *P<0.01 vs Ctl; ^#P<0.05 vs PA; ^&P<0.05 vs PA±MSP or PA±AICAR. ACC, acetyl CoA carboxylase; AMPK, AMP-activated protein kinase; Ctl, control; MSP, macrophage-stimulating protein; PA, palmitic acid; RON, recepteur d'origine nantais.