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首页> 外文期刊>Journal of Nutritional Science and Vitaminology >[6]-Gingerol Induces Amiloride-Sensitive Sodium Absorption in the Rat Colon via the Capsaicin Receptor TRPV1 in Colonic Mucosa
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[6]-Gingerol Induces Amiloride-Sensitive Sodium Absorption in the Rat Colon via the Capsaicin Receptor TRPV1 in Colonic Mucosa

机译：[6] -Gietgererol在结肠粘膜中通过辣椒素受体Trpv1诱导大鼠结肠中的余流敏感钠吸收

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摘要

[6]-Gingerol possesses various beneficial pharmacological and therapeutic properties, including anti-carcinogenic and anti-inflammatory properties and the ability to regulate intestinal contraction. Recently, our group observed that the serosal administration of [6]-gingerol stimulated electrogenic sodium absorption in the rat colon via the capsaicin receptor, TRPV1. TRPV1 is known to be expressed in both the mucosal epithelium and the muscle layers in the colon. In the present study, we assessed whether [6]-gingerol stimulated sodium absorption via TRPV1 in the colonic mucosal epithelium. We compared the effect of [6]-gingerol on TRPV1-dependent colonic sodium absorption in the colon preparation with or without muscle layer. All experiments were performed by measuring the transmural potential difference (Delta PD) in an Ussing chamber system. [6]-Gingerol induced positive Delta PD when administered to the serosal side of the colon, and this effect was significantly larger in the colon preparation without muscle layer than in that with the muscle layer. In the colon preparation without muscle layer, the [6]-gingerol-dependent induction of Delta PD was markedly suppressed by mucosal addition of amiloride, a selective inhibitor of epithelial sodium channel. APD induction by [6]-gingerol was considerably diminished by capsazepine, an inhibitor of the capsaicin receptor TRPV1, but not by AP-18, an inhibitor of TRPA1. These results suggest that [6]-gingerol induces amiloride-sensitive electrogenic sodium absorption in the rat colon via TRPV1 expressed in the colonic mucosal epithelium, and that this effect is independent of TRPV1 in the colonic muscle layer.
机译：[6] -Giglingerol具有各种有益的药理学和治疗性质，包括抗癌和抗炎性质以及调节肠道收缩的能力。最近，我们的团体观察到通过辣椒素受体，TRPV1刺激[6] -Gighterol刺激大鼠结肠中的电生钠吸收。已知TRPV1在粘膜上皮和结肠中的肌肉层中表达。在本研究中，我们评估了[6]是否通过TRPV1在结肠粘膜上皮上刺激钠吸收。我们比较了[6] -LIGNIGGEROL对具有或没有肌肉层的结肠制剂中TRPV1依赖性结肠钠吸收的影响。通过测量USSing室系统中的透射电位差（Delta PD）来进行所有实验。 [6] - 当施用于结肠的浆膜侧时， - Gighterolol诱导的正ΔPd，并且在没有肌肉层的结肠制剂中的这种效果显着大于与肌肉层的结肠制剂。在没有肌肉层的结肠制剂中，通过粘膜加入氨基吡啶酰胺的选择性抑制剂，显着抑制了δPd的[6]依赖于δPd的依赖性诱导。通过胶囊化诱导的APD诱导由辣椒蛋白酶，辣椒素受体TRPV1的抑制剂，但不是通过AP-18，TRPA1的抑制剂。这些结果表明，[6] -Giglingerol诱导在结肠粘膜上皮中表达的TRPV1在大鼠结肠中的嗜睡敏感的电钠吸收，并且这种效果与结肠肌层中的TRPV1无关。

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