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姜黄素的抗伤害作用与三磷酸腺苷敏感性钾通道的参与有关。

Evidence for the Participation of ATP-sensitive Potassium Channels in the Antinociceptive Effect of Curcumin.

机构信息

Department of Pharmacology, Center for Research and Advanced Studies of the National Polytechnic Institute, Mexico, DF, Mexico.

出版信息

Korean J Pain. 2012 Oct;25(4):221-7. doi: 10.3344/kjp.2012.25.4.221. Epub 2012 Oct 4.

Abstract

BACKGROUND

It has been reported that curcumin, the main active compound of Curcuma longa, also known as turmeric, exhibits antinociceptive properties. The aim of this study was to examine the participation of ATP-sensitive potassium channels (K(ATP) channels) and, in particular, that of the L-arginine-nitric oxide-cyclic GMP-K(ATP) channel pathway, in the antinociceptive effect of curcumin.

METHODS

Pain was induced by the intraplantar injection of 1% formalin in the right hind paw of Wistar rats. Formalin-induced flinching behavior was interpreted as an expression of nociception. The antinociceptive effect of oral curcumin was explored in the presence and absence of local pretreatment with L-NAME, an inhibitor of nitric oxide synthase, ODQ, an inhibitor of soluble guanylyl cyclase, and glibenclamide, a blocker of K(ATP) channels.

RESULTS

Oral curcumin produced a dose-dependent antinociceptive effect in the 1% formalin test. Curcumin-induced antinociception was not altered by local L-NAME or ODQ, but was significantly impaired by glibenclamide.

CONCLUSIONS

Our results confirm that curcumin is an effective antinociceptive agent. Curcumin-induced antinociception appears to involve the participation of K(ATP) channels at the peripheral level, as local injection of glibenclamide prevented its effect. Activation of K(ATP) channels, however, does not occur by activation of the L-arginine-nitric oxide-cGMP-K(ATP) channel pathway.

摘要

背景

姜黄素是姜黄的主要活性化合物,具有抗伤害感受特性。本研究旨在探讨三磷酸腺苷敏感性钾通道(K(ATP)通道),特别是精氨酸-一氧化氮-环鸟苷酸-K(ATP)通道通路,在姜黄素的抗伤害感受作用中的参与情况。

方法

通过在 Wistar 大鼠右后爪足底内注射 1%甲醛来诱导疼痛。足底内注射甲醛引起的退缩行为被解释为伤害感受的表达。在存在和不存在局部预处理的情况下,探讨了口服姜黄素的抗伤害感受作用,局部预处理包括一氧化氮合酶抑制剂 L-NAME、可溶性鸟苷酸环化酶抑制剂 ODQ 和 K(ATP)通道阻断剂 glibenclamide。

结果

口服姜黄素在 1%甲醛测试中产生了剂量依赖性的抗伤害感受作用。姜黄素诱导的抗伤害感受作用不受局部 L-NAME 或 ODQ 的影响,但被 glibenclamide 显著削弱。

结论

我们的结果证实了姜黄素是一种有效的抗伤害感受剂。姜黄素诱导的抗伤害感受作用似乎涉及外周水平的 K(ATP)通道的参与,因为局部注射 glibenclamide 阻止了其作用。然而,K(ATP)通道的激活不是通过 L-精氨酸-一氧化氮-cGMP-K(ATP)通道通路的激活来发生的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11dc/3468798/d13f0c6bec18/kjpain-25-221-g001.jpg

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