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首页> 外文期刊>Life sciences >Ultra-low dose naloxone restores the antinocicepitve effect of morphine in PTX-treated rats: Association of IL-10 upregulation in the spinal cord
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Ultra-low dose naloxone restores the antinocicepitve effect of morphine in PTX-treated rats: Association of IL-10 upregulation in the spinal cord

机译：超低剂量纳洛酮在PTX处理的​​大鼠中恢复吗啡的抗痛觉过敏作用：脊髓中IL-10上调的关联

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Aims: Ultra-low dose naloxone has been shown to restore the antinociceptive effect of morphine in pertussis toxin (PTX)-treated rats by suppressing spinal microglia activation and inhibiting inflammatory cytokine expression. This study was further investigated the mechanism by which ultra-low dose naloxone promotes analgesia in pertussis toxin-treated rats. Main methods: Male Wistar rats were implanted with an intrathecal (i.t.) catheter and injected either saline or PTX (1 μg). Four days later, rats randomly received either saline, or ultra-low dose naloxone, or recombinant rat interleukin-10 (rrIL-10) (1 μg) injection followed by saline or morphine (10 μg) 30 min later. In some experiments, mouse anti-rat IL-10 antibody (10 μg) was injected intrathecally into PTX injected rats daily on days 4, 5, 6, and 7. On day 7, ultra-low dose naloxone was given 1 h after antibody injection with or without subsequent morphine injection. Key findings: PTX injection induced notable thermal hyperalgesia and mechanical allodynia. Injection of ultra-low dose naloxone preserved the antinociceptive effect of morphine in PTX-treated rats and associated an increasing of IL-10 protein expression. Intrathecal injection rrIL-10 alone or in combination with morphine, not only reversed mechanical allodynia but also partially restored the antinociceptive effect of morphine; injection of anti-rat IL-10 antibody attenuated the effect of morphine plus ultra-low dose naloxone on mechanical allodynia and completely inhibited the antinociceptive effect of morphine. Significance: These results indicate that intrathecal ultra-low dose naloxone induces IL-10 expression in spinal neuron and microglia, which suppresses PTX-induced neuroinflammation and restores the antinociceptive effect of morphine.
机译：目的：已证明超低剂量纳洛酮可通过抑制脊髓小胶质细胞活化并抑制炎症性细胞因子的表达来恢复吗啡对百日咳毒素（PTX）治疗的大鼠的伤害感受。这项研究进一步研究了超低剂量纳洛酮促进百日咳毒素治疗大鼠镇痛的机制。主要方法：雄性Wistar大鼠植入鞘内（i.t.）导管，并注射生理盐水或PTX（1μg）。四天后，大鼠随机接受生理盐水或超低剂量纳洛酮或重组大鼠白介素10（rrIL-10）（1μg）注射，然后在30分钟后注射生理盐水或吗啡（10μg）。在某些实验中，小鼠抗大鼠IL-10抗体（10μg）在第4、5、6和7天每天鞘内注射到PTX注射的大鼠中。在第7天，抗体后1小时给予超低剂量纳洛酮注射或不注射吗啡。关键发现：PTX注射引起明显的热痛觉过敏和机械性异常性疼痛。注射超低剂量纳洛酮可保持吗啡在PTX治疗的大鼠中的镇痛作用，并与IL-10蛋白表达的增加有关。鞘内注射rrIL-10单独或与吗啡合用，不仅可以逆转机械性异常性疼痛，而且可以部分恢复吗啡的抗伤害感受作用。注射抗大鼠IL-10抗体可减弱吗啡加超低剂量纳洛酮对机械性异常性疼痛的作用，并完全抑制吗啡的抗伤害感受作用。意义：这些结果表明鞘内超低剂量纳洛酮诱导脊髓神经元和小胶质细胞中IL-10的表达，从而抑制PTX诱导的神经炎症并恢复吗啡的抗伤害感受作用。

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