Journal
FITOTERAPIA
Volume 105, Issue -, Pages 139-146Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.fitote.2015.06.005
Keywords
Rhizoma coptidis; Coptisine; Obesity; LPS; Inflammatory cytokines
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Funding
- National Science and Technology Pillar Program of China [2011BAI13B02-1]
- Chinese New Drug Institute Program of the Ministry of Science and Technology [2010ZX09401-306-3-10]
- High-end Engineering and Technical Personnel Training Plan of Chongqing
- County-University Cooperation Innovation Funds of Southwest University [Sz201401, 5z201302]
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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-alpha, 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/FLR-4-mediated signaling pathway. (C) 2015 Elsevier B.V. All rights reserved.
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