Xanthoangelol and 4-hydroxyderrcin suppress obesity-induced inflammatory responses
- Obesity (Silver Spring). 2016 Nov;24(11):2351-2360. doi: 10.1002/oby.21611.
- 1. Division of Food Science and Biotechnology, Laboratory of Molecular Function of Food, Graduate School of Agriculture, Kyoto University, Kyoto, Japan.
- 2. Research Unit for Physiological Chemistry, Japan, The Center for the Promotion of Interdisciplinary Education and Research, Kyoto University, Kyoto, Japan.
- 3. Department of Food Science and Nutrition, University of Ulsan, Ulsan, South Korea.
- 4. Division of Pharmaceutics, Osaka University of Pharmaceutical Sciences, Osaka, Japan.
- 5. Department of Bioscience, Fukui Prefectural University, Fukui, Japan.
- 6. Division of Food Science and Biotechnology, Laboratory of Molecular Function of Food, Graduate School of Agriculture, Kyoto University, Kyoto, Japan. [email protected].
- 7. Research Unit for Physiological Chemistry, Japan, The Center for the Promotion of Interdisciplinary Education and Research, Kyoto University, Kyoto, Japan. [email protected].
Objective: Obesity-induced inflammation plays a pivotal role in the pathogenesis of Insulin resistance and type 2 diabetes. Xanthoangelol (XA) and 4-hydroxyderrcin (4-HD), phytochemicals extracted from Angelica keiskei, have been reported to possess various biological properties. Whether XA and 4-HD alleviate obesity-induced inflammation and inflammation-induced adipocyte dysfunction was investigated.
Methods: For the in vitro study, a co-culture system composed of macrophages and adipocytes and macrophages stimulated with conditioned medium derived from fully differentiated adipocytes was conducted. For the in vivo study, mice were fed a high-fat diet supplemented with XA for 14 weeks.
Results: XA and 4-HD suppressed inflammatory factors in co-culture system. Moreover, treatment of RAW macrophages with XA and 4-HD moderated the suppression of uncoupling protein 1 promoter activity and gene expression in C3H10T1/2 adipocytes, which was induced by conditioned medium derived from LPS-stimulated RAW macrophages. Also, XA and 4-HD inhibited c-Jun N-terminal kinase phosphorylation, nuclear factor-κB, and activator protein 1, the last two being transcription activators in activated macrophages. Furthermore, in mice fed the high-fat diet, XA reduced inflammatory factors within the white adipose tissue.
Conclusions: These results suggest that XA and 4-HD might be promising phytochemicals to suppress obesity-induced inflammation and inflammation-induced adipocyte dysfunction.
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