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Cranberry extract attenuates hepatic inflammation in high-fat-fed obese mice
Affiliation:1. Department of Food Science, The Pennsylvania State University, University Park, PA 16802, USA;2. Department of Food Science and Technology, Virginia Polytechnic Institute and State University, Blacksburg, VA 24060, USA;3. The Center for Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, PA 16802, USA;1. Department of Applied Life Science, Faculty of Applied Biological Sciences, Gifu University, 1-1 Yanagido, Gifu-shi, Gifu 501-1193, Japan;2. Division of Life Science for Food, Department of Life Science and Chemistry, Graduate School of Natural Science and Technology, Gifu University, 1-1 Yanagido, Gifu-shi, Gifu 501-1193, Japan;3. Laboratory of Nutrition Chemistry, Department of Bioscience and Biotechnology, Faculty of Agriculture, Graduate School, Kyushu University, 744 Motooka, Nishi-ku, Fukuoka 819-0395, Japan;4. Division of Genomics Research, Life Science Research Center, Gifu University, 1-1 Yanagido, Gifu-shi, Gifu 501-1193, Japan;1. School of Food Science, Washington State University, Pullman, WA 99164, USA;2. Department of Animal Sciences, Washington State University, Pullman, WA 99164, USA;1. Facultad de Farmacia, Universidad San Pablo-CEU, Montepríncipe, Boadilla del Monte, Madrid, Spain;2. Facultad de Farmacia, Universidad de Barcelona, CIBERobn, IBUB, Barcelona, Spain;3. CQS Lab, Madrid, Spain;1. Department of Human Nutrition, Foods, and Exercise, Virginia Tech, Blacksburg, VA;2. LA Sutherland Group, LLC, Hanover, NH
Abstract:Cranberry (Vaccinium macrocarpon) consumption has been associated with health beneficial effects. Nonalcoholic fatty liver disease (NAFLD) is a comorbidity of obesity. In the present study, we investigated the effect of a polyphenol-rich cranberry extract (CBE) on hepatic inflammation in high fat (HF)-fed obese C57BL/6J mice. Following dietary treatment with 0.8% CBE for 10 weeks, we observed no change in body weight or visceral fat mass in CBE-supplemented mice compared to HF-fed control mice. We did observe a significant decrease in plasma alanine aminotransferase (31%) and histological severity of NAFLD (33% decrease in area of involvement, 29% decrease in lipid droplet size) compared to HF-fed controls. Hepatic protein levels of tumor necrosis factor α and C-C chemokine ligand 2 were reduced by 28% and 19%, respectively, following CBE supplementation. CBE significantly decreased hepatic mRNA levels of toll-like receptor 4 (TLR4, 63%) and nuclear factor κB (NFκB, 24%), as well as a number of genes related to the nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing 3 inflammasome. In conclusion, CBE reduced NAFLD and hepatic inflammation in HF-fed obese C57BL/6J mice. These effects appear to be related to mitigation of TLR4-NFκB related signaling; however, further studies into the underlying mechanisms of these hepatoprotective effects are needed.
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