触液核神经元蛋白激酶C磷酸化水平调制炎性痛大鼠的痛觉

Phosphorylation of protein kinase C in cerebrospinal fluid-contacting nucleus modulates the inflammatory pain in rats

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 present study was aimed to investigate the role of cerebrospinal fluid-contacting nucleus （CSF-CN） neurons in modulation of inflammatory pain and underlying mechanism. The inflammatory pain model was made by subcutaneous injection of the complete Freund＇s adjuvant （CFA） into the left hind paw of rats. The phosphorylation level of PKC （p-PKC） was examined by Western blot. Thermal withdrawal latency （TWL） of the rats was measured to assess inflammatory pain. The results showed that, compared with the sham controls, the inflammatory pain model rats showed shortened TWL on day 1, 3, and 7 after CFA injection, as well as increased level of p-PKC in CSF-CN neurons at 24 h after CFA injection. The administration of GF 109203X, a PKC inhibitor, into lateral ventricle decreased the level of p-PKC protein expression and increased TWL in the model rats. These results suggest that blocking the PKC pathway in CSF-CN neurons may be an effective way to reduce or eliminate the inflammatory pain.