Fig. 6.

Deficiency of leucine-rich repeat G protein-coupled receptor 4 (LGR4) renders liver more vulnerable to lipopolysaccharide/D-galactosamine (LPS/D-Gal)-induced injury. Twelve-week-old Alb-LGR4^−/− (AL) mice and wild-type (WT) littermates were injected with LPS (20 μg/kg ip) and D-Gal (400 mg/kg ip) dissolved in PBS to induce acute liver injury or with PBS in the control mice. Mice were euthanized 6 h after LPS/D-Gal injection. A: enzyme activities. Serum from WT and AL mice with PBS or LPS/D-Gal injection was used for detection of alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) enzyme activity. *P < 0.05 vs. WT+LPS/G-Gal. B: hepatic inflammatory factors. Hepatic mRNAs from animals were used for qPCR to detect expression levels of inflammatory factors. Gapdh was used as reference gene. *P < 0.05 vs. WT+LPS/G-Gal. C and D: activation of NF-κB-p65 signaling and cell death. Hepatic protein was extracted and used for Western blot to detect phospho-NF-κB-p65 and cleaved caspase-3 levels (C). TUNEL assay was performed to assay for cell death number in liver tissues (D). Green indicates TUNEL-positive cells; blue indicates nuclei; n = 6 per group. *P < 0.05 vs. WT+LPS/G-Gal.