Xiaojie Li1, Zhimeng Xu1, Shaojie Wang1, Hongli Guo1, Sizhe Dong1, Tao Wang1,2, Luyong Zhang1,3, Zhenzhou Jiang1,4. 1. Jiangsu Key Laboratory of Drug Screening, Nanjing, China. 2. Key Laboratory of Drug Quality Control and Pharmacovigilance, Ministry of Education, Nanjing, China. 3. Jiangsu Key Laboratory of TCM Evaluation and Translational Research, China Pharmaceutical University, Nanjing, China. 4. Jiangsu Center for Pharmacodynamics Research and Evaluation, Nanjing, China.
Abstract
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.
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.
Authors: Inge Mannaerts; Lien F R Thoen; Nathalie Eysackers; Francisco Javier Cubero; Sofia Batista Leite; Iain Coldham; Isabelle Colle; Christian Trautwein; Leo A van Grunsven Journal: Cell Death Dis Date: 2019-02-04 Impact factor: 8.469
Authors: Francisco J Sala de Oyanguren; Nathan E Rainey; Aoula Moustapha; Ana Saric; Franck Sureau; José-Enrique O'Connor; Patrice X Petit Journal: Cells Date: 2020-02-04 Impact factor: 6.600
Authors: Pragati Singh; Mohammad Irshad Reza; Anees A Syed; Richa Garg; Athar Husain; Roshan Katekar; Umesh K Goand; Mohammed Riyazuddin; Anand P Gupta; Jiaur R Gayen Journal: Heliyon Date: 2020-12-29