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

Aim To 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. Methods Sprague–Dawley rats were divided into the control, fructose‐feeding group, and three fructose‐feeding groups treated with 40, 80 and 160 mg/kg emodin, respectively. After 4 weeks 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. Results Emodin 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. Conclusion Emodin is capable of improving the lipid accumulation through the ERS–SREBP1c pathway in fructose‐induced non‐alcoholic fatty liver disease.