Yu, JunChu, Eagle S. H.Hui, Alex Y.Cheung, Kin FChan, Henry L. Y.Leung, Wai K.Farrell, GeoffreySung, Joseph J Y2015-12-070006-291Xhttp://hdl.handle.net/1885/28306Dietary model of steatohepatitis was established by feeding mice a methionine choline deficient (MCD) diet. Mice on MCD or control diet for 3 weeks were treated with or without NO-1886, a newly synthetic lipoprotein lipase (LPL) activator. In a separate experiment, NO-1886 was given after pre-treatment with 3 weeks of MCD diet. NO-1886 significantly reduced MCD-induced inflammation by repressing levels of hepatic lipid peroxides and pro-inflammatory tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and cyclooxygenase-2 (COX-2). In addition, NO-1886 dampened hepatic steatosis via accelerating fatty acid oxidation caused by enhanced expression of PPARα, cytochrome P450-10 (Cyp4a10), and Acyl-CoA oxidase (ACO). It failed to regulate genes of fatty acid uptake and synthesis pathways. In conclusion, NO-1886 ameliorated and induced regression of experimental steatohepatitis via increasing endogenous LPL activation resulting in suppression on pro-inflammatory factors and reduction of hepatic fatty acids. These findings indicate that NO-1886 is a potential therapeutic agent for steatohepatitis.Keywords: 4 [(4 bromo 2 cyanophenyl)carbamoyl]benzylphosphonic acid diethyl ester; acyl coenzyme A oxidase; choline; cyclooxygenase 2; cytochrome P450 4A; cytochrome p450 4a10; fatty acid; interleukin 6; lipid peroxide; lipoprotein lipase; methionine; peroxisome pr Cytokines; Lipoprotein lipase; NO-1886; Nutritional steatohepatitis; Peroxisome proliferator-activated receptor200710.1016/j.bbrc.2007.02.1292015-12-07