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Green Tea Polyphenol Epigallocatechin Gallate Activates TRPA1 in an Intestinal Enteroendocrine Cell Line, STC-1

机译:绿茶多酚表没食子儿茶素没食子酸酯可激活肠内分泌细胞系STC-1中的TRPA1。

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摘要

A characteristic astringent taste is elicited by polyphenols. Among the polyphenols, catechins and their polymers are the most abundant polyphenols in wine and tea. A typical green tea polyphenol is epigallocatechin gallate (EGCG). Currently, the mechanism underlying the sensation of astringent taste is not well understood. We observed by calcium imaging that the mouse intestinal endocrine cell line STC-1 responds to the astringent compound, EGCG. Among major catechins of green tea, EGCG was most effective at eliciting a response in this cell line. This cellular response was not observed in HEK293T or 3T3 cells. Further analyses demonstrated that the 67-kDa laminin receptor, a known EGCG receptor, is not directly involved. The Ca2+ response to EGCG in STC-1 cells was decreased by inhibitors of the transient receptor potential A1 (TRPA1) channel. HEK293T cells transfected with the mouse TRPA1 (mTRPA1) cDNA showed a Ca2+ response upon application of EGCG, and their response properties were similar to those observed in STC-1 cells. These results indicate that an astringent compound, EGCG, activates the mTRPA1 in intestinal STC-1 cells. TRPA1 might play an important role in the astringency taste on the tongue.
机译:多酚可引起典型的涩味。在多酚中,儿茶素及其聚合物是酒和茶中含量最丰富的多酚。典型的绿茶多酚是表没食子儿茶素没食子酸酯(EGCG)。目前,对涩味感觉的潜在机制尚不十分了解。我们通过钙成像观察到,小鼠肠道内分泌细胞系STC-1对收敛性化合物EGCG作出反应。在绿茶的主要儿茶素中,EGCG在引起这种细胞系反应方面最有效。在HEK293T或3T3细胞中未观察到这种细胞反应。进一步的分析表明,已知的EGCG受体67 kDa层粘连蛋白受体不直接参与。瞬时受体电位A1(TRPA1)通道的抑制剂降低了STC-1细胞对EGCG的Ca 2 + 反应。转染小鼠TRPA1(mTRPA1)cDNA的HEK293T细胞在应用EGCG时显示Ca 2 + 反应,其反应特性与STC-1细胞相似。这些结果表明,收敛性化合物EGCG可激活肠道STC-1细胞中的mTRPA1。 TRPA1可能在舌头的涩味中起重要作用。

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  • 来源
    《Chemical Senses》 |2012年第2期|p.167-177|共11页
  • 作者单位

    1Department of Bio-Science, Faculty of Bio-Science, Nagahama Institute of Bio-Science and Technology, 1266 Tamura-cho, Nagahama-shi, Shiga 526-0829, Japan 2Division of Biophysics and Neurobiology, Department of Molecular Physiology, National Institute for Physiological Sciences, 38 Nishigonaka, Myodaiji, Okazaki, Aichi 444-8585, Japan;

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