姜黄素诱导的神经病理性痛觉过敏的抗作用是通过 NO-cGMP-ATP 敏感的钾通道途径介导的。

Anti-allodynic effect induced by curcumin in neuropathic rat is mediated through the NO-cyclic-GMP-ATP sensitive K channels pathway.

机构信息

Departamento de Sistemas Biológicos, División de Ciencias Biológicas y de la Salud, Universidad Autónoma Metropolitana-Xochimilco, Calzada del Hueso 1100, Colonia Villa Quietud, 04960, Mexico, D.F., Mexico.

Departamento de Matemáticas, Facultad de Ciencias, Universidad Nacional Autónoma de México, CDMX, Apartado Postal 20-726, 01000, México, Mexico.

出版信息

BMC Complement Med Ther. 2020 Mar 14;20(1):83. doi: 10.1186/s12906-020-2867-z.

DOI:10.1186/s12906-020-2867-z

PMID:32171311

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7076866/

Abstract

BACKGROUND

Recent studies pointed up that curcumin produces an anti-nociceptive effect in inflammatory and neuropathic pain. However, the possible mechanisms of action that underline the anti-allodynic effect induced by curcumin are not yet established. The purpose of this study was to determine the possible anti-allodynic effect of curcumin in rats with L5-L6 spinal nerve ligation (SNL). Furthermore, we study the possible participation of the NO-cyclic GMP-ATP-sensitive K channels pathway in the anti-allodynic effect induced by curcumin.

METHODS

Tactile allodynia was measured using von Frey filaments by the up-down method in female Wistar rats subjected to SNL model of neuropathic pain.

RESULTS

Intrathecal and oral administration of curcumin prevented, in a dose-dependent fashion, SNL-induced tactile allodynia. The anti-allodynic effect induced by curcumin was prevented by the intrathecal administration of L-NAME (100 μg/rat, a non-selective nitric oxide synthase inhibitor), ODQ (10 μg/rat, an inhibitor of guanylate-cyclase), and glibenclamide (50 μg/rat, channel blocker of ATP-sensitive K channels).

CONCLUSIONS

These data suggest that the anti-allodynic effect induced by curcumin is mediated, at least in part, by the NO-cyclic GMP-ATP-sensitive K channels pathway in the SNL model of neuropathic pain in rats.

摘要

背景

最近的研究表明，姜黄素在炎症和神经病理性疼痛中产生抗伤害感受作用。然而，姜黄素诱导的抗痛觉过敏作用的可能作用机制尚未确定。本研究旨在确定姜黄素在 L5-L6 脊神经结扎（SNL）大鼠中产生抗痛觉过敏的可能性。此外，我们研究了 NO-cGMP-ATP 敏感钾通道途径在姜黄素诱导的抗痛觉过敏作用中的可能参与。