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6-姜烯酚和6-姜酚是生姜中的辛辣成分,它们通过不同机制抑制3T3-L1脂肪细胞中肿瘤坏死因子-α介导的脂联素表达下调。

6-Shogaol and 6-gingerol, the pungent of ginger, inhibit TNF-alpha mediated downregulation of adiponectin expression via different mechanisms in 3T3-L1 adipocytes.

作者信息

Isa Yasuka, Miyakawa Yuri, Yanagisawa Masayoshi, Goto Tsuyoshi, Kang Min-Sook, Kawada Teruo, Morimitsu Yasujiro, Kubota Kikue, Tsuda Takanori

机构信息

College of Bioscience and Biotechnology, Chubu University, Kasugai, 1200 Matsumoto-cho, Kasugai, Aichi 487-8501, Japan.

出版信息

Biochem Biophys Res Commun. 2008 Aug 29;373(3):429-34. doi: 10.1016/j.bbrc.2008.06.046. Epub 2008 Jun 23.

DOI:10.1016/j.bbrc.2008.06.046
PMID:18577375
Abstract

In this study, we demonstrated that the two ginger-derived components have a potent and unique pharmacological function in 3T3-L1 adipocytes via different mechanisms. Both pretreatment of 6-shogaol (6S) and 6-gingerol (6G) significantly inhibited the tumor necrosis factor-alpha (TNF-alpha) mediated downregulation of the adiponectin expression in 3T3-L1 adipocytes. Our study demonstrate that (1) 6S functions as a PPARgamma agonist with its inhibitory mechanism due to the PPARgamma transactivation, and (2) 6G is not a PPARgamma agonist, but it is an effective inhibitor of TNF-alpha induced c-Jun-NH(2)-terminal kinase signaling activation and thus, its inhibitory mechanism is due to this inhibitory effect.

摘要

在本研究中,我们证明了两种源自姜的成分通过不同机制在3T3-L1脂肪细胞中具有强大且独特的药理功能。6-姜辣素(6S)和6-姜酚(6G)的预处理均显著抑制肿瘤坏死因子-α(TNF-α)介导的3T3-L1脂肪细胞中脂联素表达的下调。我们的研究表明:(1)6S作为一种PPARγ激动剂,其抑制机制归因于PPARγ反式激活;(2)6G不是PPARγ激动剂,但它是TNF-α诱导的c-Jun-NH₂-末端激酶信号激活的有效抑制剂,因此,其抑制机制归因于这种抑制作用。

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