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本研究旨在探讨触液核在炎性疼痛中的作用及其机制。用大鼠左侧足底皮下注射完全弗氏佐剂(complete Freund’s adjuvant,CFA)来建立炎性痛模型,用Western blot检测炎性痛模型大鼠触液核中蛋白激酶C(protein kinase C,PKC)磷酸化水平的变化,用热缩足反射潜伏期(thermal withdrawal latency,TWL)检测来了解大鼠炎性痛觉情况。结果显示,炎性痛大鼠CFA注射后第1、3和7天TWL显著降低,注射CFA后24 h时触液核中p-PKC蛋白水平显著高于正常对照大鼠;侧脑室注射PKC抑制剂GF109203X可降低炎性痛大鼠触液核PKC磷酸化水平并提高痛觉阈值。以上结果提示,阻断触液核中PKC通路的信号转导可能是减轻或消除炎性痛的有效手段。
The purpose of this study was to investigate the role and mechanism of the fluid-induced nucleus in inflammatory pain. Inflammatory pain model was established by subcutaneous injection of complete Freund’s adjuvant (CFA) on the left foot of rats, and Western blot was used to detect the protein kinase C PKC) phosphorylation, we used the thermal withdrawal latency (TWL) test to understand the inflammatory pain in rats. The results showed that TWA was significantly decreased on the 1st, 3rd, and 7th day after injection of CFA in inflammatory pain rats, and the level of p-PKC protein in the liquid nucleus 24 hours after CFA injection was significantly higher than that in the normal control rats. The intracerebroventricular injection of PKC inhibited Agent GF109203X can reduce PKC phosphorylation and increase the threshold of pain threshold in inflammatory pain rats. The above results suggest that blocking the signal transduction of the PKC pathway in the palpable fluid may be an effective means of reducing or eliminating inflammatory pain.