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黄嘌呤醇和4-羟基德里辛可抑制肥胖诱导的炎症反应。

Xanthoangelol and 4-hydroxyderrcin suppress obesity-induced inflammatory responses.

作者信息

Li Yongjia, Goto Tsuyoshi, Ikutani Ryuma, Lin Shan, Takahashi Nobuyuki, Takahashi Haruya, Jheng Huei-Fen, Yu Rina, Taniguchi Masahiko, Baba Kimiye, Murakami Shigeru, Kawada Teruo

机构信息

Division of Food Science and Biotechnology, Laboratory of Molecular Function of Food, Graduate School of Agriculture, Kyoto University, Kyoto, Japan.

Research Unit for Physiological Chemistry, Japan, The Center for the Promotion of Interdisciplinary Education and Research, Kyoto University, Kyoto, Japan.

出版信息

Obesity (Silver Spring). 2016 Nov;24(11):2351-2360. doi: 10.1002/oby.21611. Epub 2016 Sep 13.

DOI:10.1002/oby.21611
PMID:27619735
Abstract

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.

摘要

目的

肥胖诱导的炎症在胰岛素抵抗和2型糖尿病的发病机制中起关键作用。据报道,从明日叶中提取的植物化学成分黄当归醇(XA)和4-羟基德里辛(4-HD)具有多种生物学特性。本研究旨在探讨XA和4-HD是否能减轻肥胖诱导的炎症以及炎症诱导的脂肪细胞功能障碍。

方法

体外研究采用巨噬细胞与脂肪细胞共培养系统,以及用完全分化的脂肪细胞条件培养基刺激巨噬细胞。体内研究中,给小鼠喂食含XA的高脂饮食14周。

结果

XA和4-HD在共培养系统中抑制炎症因子。此外,用XA和4-HD处理RAW巨噬细胞可减轻LPS刺激的RAW巨噬细胞条件培养基诱导的C3H10T1/2脂肪细胞解偶联蛋白1启动子活性和基因表达的抑制。而且,XA和4-HD抑制c-Jun氨基末端激酶磷酸化、核因子-κB和激活蛋白1,后两者是活化巨噬细胞中的转录激活因子。此外,在喂食高脂饮食的小鼠中,XA减少了白色脂肪组织中的炎症因子。

结论

这些结果表明,XA和4-HD可能是有前景的植物化学成分,可抑制肥胖诱导的炎症和炎症诱导的脂肪细胞功能障碍。

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