Fig. 1: Lack of GPR120 exacerbated, whereas activation of GPR120 ameliorated, the severity of bacteria-induced liver injury.

Wild-type (WT) and GPR120−/− (GPR120 KO) mice were injected with P. acnes (P.ac) suspended in 100 μL of PBS. Vehicle or TUG891 (10 mg/kg) was administered i.p. to WT primed mice on days 0, 2, 4, and 6 (n = 7 mice per group). a One microgram of LPS in 100 μL of PBS was injected into all P. acnes-primed mice on day 7 to aggravate FHF. Cumulative survival rates were analyzed. b Liver and spleen tissues were isolated and photographed. Representative images from one of three experiments were shown. c The weights of livers and spleens from the four groups was measured. d Serum was collected on day 7, and the levels of ALT and AST were measured. e Liver tissues were sectioned for histological examination and semiquantitative analysis of inflammatory conditions in the liver were shown. Scale bar, 100 μm. f Frozen sections of livers were used for TUNEL staining. Scale bar, 100 μm. The results are representative of three to six independent experiments and presented as the mean ± SEM. Significant differences were analyzed by Log-rank test (a), One-way ANOVA (b–f). *p < 0.05, **p < 0.01, ***p < 0.001.