title: Coptisine attenuates obesity-related inflammation through LPS/TLR-4-mediated signaling pathway in Syrian golden hamsters.
abstract: It is known that obesity resulted from consumption of diets high in fat and calories and associated with a chronic low-grade inflammation. Because the fat, sterol and bile acid metabolism of male Syrian golden hamster are more similar to that of human, in the present study, high fat and high cholesterol (HFHC) induced obese hamsters were used to evaluate the anti-inflammation and hypolipidemic role of coptisine. The results showed that body weight, plasma lipid levels of total cholesterol (TC), triglyceride (TG), low density lipoprotein-cholesterol (LDL-c), very low density lipoprotein-cholesterol (VLDL-c), ApoB and pro-inflammatory cytokines including TNF-α, IL-6 and lipopolysaccharide (LPS) were significantly altered in hamsters fed with HFHC diet. A strong correlation was observed between the LPS level in serum and the level of LBP and pro-inflammatory cytokines. Coptisine from the concentrations of 60 to 700 mg/L dose-dependently inhibited Enterobacter cloacae growth, which can easily induce obesity and insulin resistance. The results of endotoxin neutralization assay suggest that coptisine is capable of reducing the LPS content under inflammation status. Real time RT-PCR analyses revealed that coptisine suppressed TLR-4 in visceral fat of hamsters and decreased CD14 expression in livers of hamsters. These encouraging findings make the development of coptisine a good candidate for preventing obesity-related diseases through the LPS/TLR-4-mediated signaling pathway.
authors.affiliation: College of Pharmaceutical Sciences, Southwest University, Chongqing, China; Chongqing Productivity Promotion Centre for Modern Chinese Medicine, Chongqing, China.
authors.forename: Zong-Yao
authors.initials: ZY
authors.lastname: Zou
authors.affiliation: College of Pharmaceutical Sciences, Southwest University, Chongqing, China; Chongqing Productivity Promotion Centre for Modern Chinese Medicine, Chongqing, China.
authors.forename: Yin-Ran
authors.initials: YR
authors.lastname: Hu
authors.affiliation: College of Pharmaceutical Sciences, Southwest University, Chongqing, China; Chongqing Productivity Promotion Centre for Modern Chinese Medicine, Chongqing, China.
authors.forename: Hang
authors.initials: H
authors.lastname: Ma
authors.affiliation: College of Pharmaceutical Sciences, Southwest University, Chongqing, China; Chongqing Productivity Promotion Centre for Modern Chinese Medicine, Chongqing, China.
authors.forename: Yan-Zhi
authors.initials: YZ
authors.lastname: Wang
authors.affiliation: College of Pharmaceutical Sciences, Southwest University, Chongqing, China; Chongqing Productivity Promotion Centre for Modern Chinese Medicine, Chongqing, China.
authors.forename: Kai
authors.initials: K
authors.lastname: He
authors.affiliation: College of Pharmaceutical Sciences, Southwest University, Chongqing, China; Chongqing Productivity Promotion Centre for Modern Chinese Medicine, Chongqing, China.
authors.forename: Shuang
authors.initials: S
authors.lastname: Xia
authors.affiliation: School of Life Sciences, Southwest University, Chongqing, China.
authors.forename: Hao
authors.initials: H
authors.lastname: Wu
authors.affiliation: School of Life Sciences, Southwest University, Chongqing, China.
authors.forename: Dong-Fang
authors.initials: DF
authors.lastname: Xue
authors.affiliation: College of Pharmaceutical Sciences, Southwest University, Chongqing, China; Chongqing Productivity Promotion Centre for Modern Chinese Medicine, Chongqing, China. Electronic address: Xuegangli@swu.edu.cn.
authors.forename: Xue-Gang
authors.initials: XG
authors.lastname: Li
authors.affiliation: School of Life Sciences, Southwest University, Chongqing, China. Electronic address: yexiaoli@swu.edu.cn.
authors.forename: Xiao-Li
authors.initials: XL
authors.lastname: Ye
mesh_terms: D000818:Animals; D001599:Berberine / Q000031:analogs & derivatives* / Q000494:pharmacology; D001835:Body Weight / Q000187:drug effects; D002784:Cholesterol / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D039323:Coptis / Q000737:chemistry; D059305:Diet, High-Fat; D004195:Disease Models, Animal; D007249:Inflammation / Q000188:drug therapy*; D015850:Interleukin-6 / Q000097:blood; D050356:Lipid Metabolism; D058635:Lipid-Linked Proteins; D008070:Lipopolysaccharides / Q000097:blood; D008297:Male; D008647:Mesocricetus; D015394:Molecular Structure; D009765:Obesity / Q000188:drug therapy / Q000503:physiopathology*; D015398:Signal Transduction; D051197:Toll-Like Receptor 4 / Q000378:metabolism*; D014280:Triglycerides / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D008078:Cholesterol, LDL; D015850:Interleukin-6; D058635:Lipid-Linked Proteins; D008070:Lipopolysaccharides; D051197:Toll-Like Receptor 4; D014280:Triglycerides; D014409:Tumor Necrosis Factor-alpha; C034384:coptisine; D001599:Berberine; D002784:Cholesterol
keywords: Coptisine; Coptisine (PubChem CID: 72322); Inflammatory cytokines; LPS; Obesity; Orlistat (PubChem CID: 3034010); Rhizoma coptidis