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

中文翻译：

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姜黄素在神经病大鼠中诱导的抗异常疼痛作用是通过 NO-cycl-GMP-ATP 敏感 K+ 通道途径介导的。

最近的研究指出，姜黄素对炎症和神经性疼痛具有抗伤害作用。然而，强调姜黄素引起的抗异常疼痛作用的可能作用机制尚未确定。本研究的目的是确定姜黄素对 L5-L6 脊髓神经结扎 (SNL) 大鼠可能的抗异常疼痛作用。此外，我们研究了 NO-环状 GMP-ATP 敏感 K+ 通道通路在姜黄素诱导的抗异常疼痛作用中的可能参与。在接受 SNL 神经性疼痛模型的雌性 Wistar 大鼠中，使用 von Frey 丝通过上下法测量触觉异常性疼痛。鞘内和口服姜黄素以剂量依赖性方式预防 SNL 引起的触觉异常性疼痛。鞘内注射 L-NAME（100 μg/大鼠，一种非选择性一氧化氮合酶抑制剂）、ODQ（10 μg/大鼠，鸟苷酸环化酶抑制剂）和格列本脲（50 μg/大鼠，ATP 敏感 K+ 通道的通道阻滞剂）。这些数据表明，在大鼠神经性疼痛的 SNL 模型中，姜黄素诱导的抗异常疼痛作用至少部分是由 NO-环 GMP-ATP 敏感 K+ 通道通路介导的。