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首页> 外文期刊>BMC Complementary and Alternative Medicine >Anti-allodynic effect induced by curcumin in neuropathic rat is mediated through the NO-cyclic-GMP-ATP sensitive K channels pathway
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Anti-allodynic effect induced by curcumin in neuropathic rat is mediated through the NO-cyclic-GMP-ATP sensitive K channels pathway

机译:姜黄素诱导的神经疗法大鼠诱导的抗异点效果通过NO-CNAP-GMP-ATP敏感K通道介导

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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.
机译:最近的研究指出,姜黄素在炎症和神经病疼痛中产生抗伤害效果。然而,尚未建立强调由姜黄素诱导的抗异点效果的可能作用机制。本研究的目的是确定姜黄素在L5-L6脊神经连接(SN1)的大鼠中可能的抗病变量效果。此外,我们研究了No-Cyclic GMP-ATP-ATP敏感K通道途径在姜黄素诱导的抗分解效果中的可能参与。使用von Frey长丝测量触觉异常,通过对神经病疼痛的SNL模型进行的女性Wistar大鼠的上下方法测量。鞘内和口服姜黄素施用,以剂量依赖性的方式,SNL诱导的触觉异常性疼痛。通过鞘内施用L-名称(100〜μg/大鼠,非选择性一氧化氮合酶抑制剂),ODQ(10〜μg/大鼠,胍酸酯环酶抑制剂)来防止由姜黄素诱导的抗异点效应和Glibenclamide(50μg/大鼠,ATP敏感k通道的通道阻滞剂)。这些数据表明,姜黄素诱导的抗异点效果至少部分地由大鼠神经性疼痛的SNL模型中的No-Cyclic GMP-ATP敏感K通道介导。

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