非甾体类抗炎药减轻大鼠颞下颌关节炎症诱导后的痛觉过敏,阻断三叉神经节钠通道1.7的上调。

Rui-yun Bi, Yun Ding, Y. Gan
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引用次数: 10

摘要

目的探讨非甾体抗炎药(NSAIDs)镇痛作用与三叉神经节(TG)钠通道1.7 (Nav1.7)表达的关系。方法采用完全弗氏佐剂(CFA)诱导雌性大鼠颞下颌关节(TMJ)炎症。诱导TMJ炎症前ig布洛芬、双氯芬酸钠、美洛昔康。采用TMJ炎症的组织病理学评估和评分来评估炎症程度。测量头部戒断阈值和食物摄取量以评估颞下颌关节伤害性反应。采用实时聚合酶链反应和western blot检测三叉神经节Nav1.7 mRNA和蛋白的表达。结果非甾体抗炎药(NSAIDs)在TMJ内注射CFA 24 h后,减轻了炎症TMJ的痛觉过敏,同时阻断了炎症诱导的TG中Nav1.7 mRNA和蛋白表达上调。然而,布洛芬和双氯芬酸钠轻度减轻TMJ炎症,美洛昔康对TMJ炎症无影响。结论非甾体抗炎药对炎性TMJ痛觉过敏的抑制作用可能与其阻断三叉神经节Nav1.7上调有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Non-steroidal Anti-inflammatory Drugs Attenuate Hyperalgesia and Block Upregulation of Trigeminal Ganglionic Sodium Channel 1.7 after Induction of Temporomandibular Joint Inflammation in Rats.
OBJECTIVE To investigate the association between the analgesic effect of non-steroidal antiinflammatory drugs (NSAIDs) and sodium channel 1.7 (Nav1.7) expression in the trigeminal ganglion (TG). METHODS Temporomandibular joint (TMJ) inflammation was induced by complete Freund's adjuvant (CFA) in female rats. Ibuprofen, diclofenac sodium and meloxicam were given intragastrically before induction of TMJ inflammation. Histopathological evaluation and scoring of TMJ inflammation was used to evaluate the level of inflammation. The head withdrawal threshold and food intake were measured to evaluate TMJ nociceptive responses. The mRNA and protein expression of trigeminal ganglionic Nav1.7 was examined using real-time polymerase chain reaction and western blot. RESULTS Twenty-four hours after the injection of CFA into the TMJs, NSAIDs attenuated hyperalgesia of inflamed TMJ and simultaneously blocked inflammation-induced upregulation of Nav1.7 mRNA and protein expression in the TG. However, ibuprofen and diclofenac sodium slightly attenuated TMJ inflammation and meloxicam did not affect TMJ inflammation. CONCLUSION Attenuation of hyperalgesia of inflamed TMJ by NSAIDs might be associated with their role in blocking upregulation of trigeminal ganglionic Nav1.7.
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