Results: Result 1. LPS induced live injury with increased PF-01367338 ic50 serum ALT, AST, and TNF levels, high histological injury score, apoptosis of hepatocytes, accumulation of macrophage and neutrophil evidenced with increment of CD68 expression and MPO activity
in liver.2. AICAR or compound C treatment decreased ALT, AST, and TNF levels in serum, reduced histological injury score, CD68 expression, MPO activity, apoptosis cell number in liver of mice with endotoxemia. However, combination of AICAR and compound C treatments failed to exhibit the benefit effect of each single treatment.3. In survival experiments, AICAR or compound C treatment improved survival of endotoxemic mice. Conclusion: ConclusionAICAR or compound C treatment attenuates LPS-induced liver dysfunction, indicating that activation of inhibition AMPK signal can inhibit endotoxemia-induced immune response and liver injury. AMPK signal may provide an alternative to the current clinical treatments for endotoxemia. Key Word(s): 1. Endotoxemia; 2. AMPK; 3. AICAR; 4. liver damage; Presenting Author: HUITING GAO Additional Authors: LISHU
XU, LICHANG GUAN, DONGFENG LI, WEIPING DENG Corresponding Author: LISHU XU Affiliations: Guangdong General selleck chemicals llc Hospital Objective: The aims of the study were to investigate the effect of glucagon-like peptide-1 (GLP-1) on diet induce non-alcoholic fatty liver disease (NAFLD) in rats. Methods: A total of 30 male rats were randomly divided into three groups. Each group contained 10 rats, in which they were fed with normal diet (ND), high-fat diet (HFD), high-fat diet with intraperitoneal injection of liraglutide (HFD+GLP-1, first 12 weeks with HFD, later 4 weeks with liraglutide) for 16 weeks respectively. After 16 weeks’ feeding, the rats were killed ethically and their blood samples and liver tissues were collected. The levels of aminotransferase (ALT), aspartate-aminotransferase (AST), triglyceride (TG), total-cholesterol 上海皓元医药股份有限公司 (TC) were detected by biochemistry automatic analyzer. The levels of superoxide dismutase (SOD)
and malondial-dehyde (MAD), tumor necrosis factor-a (TNF-a), JNK-1 and P-JNK1 in liver homogenates were detected by RIA, ELISA and Western blot respectively. Results: The body weight, liver index, serum and liver homogenates levels of TG, TC, ALT and TG, TC, MAD, TNF-a in the HFD group were apparently higher than those in the normal group, while the level of SOD decreased significantly. When compared with the HFD group, the body weight, liver index, serum and liver homogenates levels of TG, TC, ALT and TG, TC, MAD, TNF-a in the HFD+GLP-1 group decreased apparently, while the level of SOD increased. (P < 0.05) Conclusion: Liraglutide (GLP-1) has an anti-inflammatory effect on NAFLD rats, which is conducted by decreasing blood lipid and liver homogenate inflammation index level. Key Word(s): 1. NAFLD; 2. GLP-1; 3.