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通过观察完全弗氏佐剂(complete Freund’s adjuvant,CFA)炎症痛大鼠对伤害性热刺激的缩足反射潜伏期(paw withdrawal latency,PWL)变化,探讨Gi蛋白是否介导MrgC受体(Mas-related gene C receptors,MrgC)对炎症痛的抗痛觉过敏作用.结果显示,椎管内给予MrgC受体激动剂BAM8-22(bovine adrenal medulla 8-22,BAM8-22)能明显延长CFA炎症鼠在24 h和48 h时的缩足反射潜伏期基础值,并显著增强24h时的抗伤害作用.椎管内预先给予百日咳毒素(pertussis toxin,PTX)能抑制Gi蛋白的功能.在给予PTX7 d后,初次给予BAM8-22并不能延长CFA炎症鼠24 h时的缩足潜伏期基础值,但在24 h时再次注射BAM8-22时,能显著增强其抗伤害作用和48 h时的缩足潜伏期基础值.以上结果说明在CFA炎症痛模型中,预先给予PTX能抑制BAM8-22的抗痛觉过敏作用,但重复再次给予BAM8-22能恢复Gi蛋白的功能.表明Gi蛋白及其相关信号通路介导MrgC受体在炎症痛中的抗痛觉过敏作用.
By observing the changes of paw withdrawal latency (PWL) in noxious heat-stimulated rats with complete Freund’s adjuvant (CFA) to investigate whether Gi protein mediates MrgC receptor (Mas-related gene C receptors, MrgC) on inflammatory pain.Results showed that administration of Bg8-22 (bovine adrenal medulla 8-22, BAM8-22) h and 48 h, and significantly increased the anti-injury effect at 24h.The pretreatment with pertussis toxin (PTX) in spinal canal could inhibit the function of Gi protein.After PTX7 d, Administration of BAM8-22 did not prolong the baseline value of 24 h contraction in CFA-inflamed rats. However, BAM8-22 injected at 24 h significantly enhanced its anti-injury effect and the baseline value of hypoplasia latency at 48 h. The above results indicate that pretreatment with PTX can inhibit the anti-hyperalgesia of BAM8-22 in CFA inflammatory pain model, but the repeated administration of BAM8-22 can restore the function of Gi protein, indicating that Gi protein and its related signaling pathways mediate MrgC Anti-allodynia in inflammatory pain Allergic effects.