Introduction Lutein is a dietary constituent known to inhibit inflammation; however, its effect on nociceptive neuron-associated hyperalgesia remains to be determined. The present study therefore investigated under in vivo conditions whether administration of lutein attenuates the inflammation-induced hyperexcitability of trigeminal spinal nucleus caudalis (SpVc) neurons that is associated with mechanical hyperalgesia. Results Complete Freund's adjuvant (CFA) was injected into the whisker pads of rats to induce inflammation, and then mechanical stimulation was applied to the orofacial area to assess the threshold of escape. The mechanical threshold was significantly lower in inflamed rats compared to uninjected naïve rats, and this lowered threshold was returned to control levels by 3 days after administration of lutein (10 mg/Kg, i.p.) Also the lutein administration, inflammation-induced thickness of edema was returned to control levels. The mean increased number of cyclooxygenase-2 (Cox-2)-immunoreactive cells in the whisker pads of inflamed rats was also returned to control levels by administration with lutein. The mean discharge frequency of SpVc wide-dynamic range (WDR) neurons to both nonnoxious and noxious mechanical stimuli in inflamed rats was significantly decreased after lutein administration. In addition, the increased mean spontaneous discharge of SpVc WDR in inflamed rats was significantly decreased after lutein administration. Similarly, lutein significantly diminished noxious pinch-evoked mean after discharge frequency and occurrence in inflamed rats. Finally, lutein restored the expanded mean size of the receptive field in inflamed rats to control levels. Conclusion These results together suggest that administration of lutein attenuates inflammatory hyperalgesia associated with hyperexcitability of nociceptive SpVc WDR neurons via inhibition of the peripheral Cox-2 signaling cascade. These findings support the proposed potential of lutein as a therapeutic agent in complementary alternative medicine strategies for preventing inflammatory mechanical hyperalgesia.

中文翻译：

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通过抑制环氧合酶 2 级联信号传导，全身给予叶黄素后，抑制与炎症痛觉过敏相关的三叉神经伤害性神经元的过度兴奋。


简介 叶黄素是一种已知能抑制炎症的膳食成分；然而，其对伤害性神经元相关痛觉过敏的影响仍有待确定。因此，本研究在体内条件下调查了叶黄素的施用是否可以减弱炎症诱导的三叉神经尾髓核（SpVc）神经元的过度兴奋性，而该神经元与机械性痛觉过敏相关。结果将完全弗氏佐剂（CFA）注射到大鼠的胡须垫中诱导炎症，然后对口面部区域施加机械刺激以评估逃避阈值。与未注射的幼稚大鼠相比，发炎大鼠的机械阈值显着降低，并且在施用叶黄素（10 mg/Kg，腹膜内）后 3 天，这种降低的阈值恢复到对照水平。已恢复至控制水平。通过给予叶黄素，发炎大鼠胡须垫中环氧合酶-2 (Cox-2) 免疫反应细胞的平均增加数量也恢复到对照水平。给予叶黄素后，发炎大鼠的 SpVc 宽动态范围 (WDR) 神经元对非伤害性和伤害性机械刺激的平均放电频率显着降低。此外，给予叶黄素后，发炎大鼠中增加的 SpVc WDR 平均自发放电显着降低。类似地，叶黄素显着减少了发炎大鼠放电频率和发生后的有害捏诱发平均数。最后，叶黄素使发炎大鼠感受野的平均大小恢复到控制水平。 结论 这些结果共同表明，叶黄素的施用通过抑制外周 Cox-2 信号级联来减轻与伤害性 SpVc WDR 神经元过度兴奋相关的炎症痛觉过敏。这些发现支持了叶黄素作为预防炎症性机械痛觉过敏的补充替代医学策略中的治疗剂的潜力。