Emodin ameliorates hepatic steatosis through endoplasmic reticulum-stress sterol regulatory element-binding protein 1c pathway in liquid fructose-feeding rats

AimTo investigate the effects of emodin on the treatment of non-alcoholic fatty liver in rats induced by liquid fructose-feeding in rats and the possible underlying mechanisms. MethodsSprague-Dawley rats were divided into the control, fructose-feeding group, and three fructose-feeding groups treated with 40, 80 and 160mg/kg emodin, respectively. After 4weeks of feeding, liquid consumption, food intake, bodyweight, liver index, serum triglyceride (TG), glucose and aminotransferases (aspartate aminotransferase [AST] and alanine aminotransferase [ALT]), liver TG contents and histology features were examined. The hepatic expression of lipogenic and fatty acid oxidation key enzymes, and an upstream transcriptional factor, sterol regulatory element-binding protein 1c (SREBP1c) were determined. Glucose regulated protein 78 (GRP78), a liver endoplasmic reticulum stress (ERS) marker and the unfolded protein response (UPR) related proteins were also measured. ResultsEmodin reduced bodyweight, liver index, serum TG levels of fructose-feeding rats with no significant difference in serum glucose, AST and ALT levels. Emodin improved hepatic steatosis by inhibiting SREBP1c activation and its target genes, and enhancing carnitine palmitoyltransferase 1 expression in fructose-feeding rats. Emodin resolved hepatic ERS and the UPR induced by liquid fructose in rats. ConclusionEmodin is capable of improving the lipid accumulation through the ERS-SREBP1c pathway in fructose-induced non-alcoholic fatty liver disease.