NK-1受体拮抗剂CP-96345对关节炎大鼠痛行为和IL-1β mRNA表达的影响

The Effect of NK-1 Receptor Antagonist CP 96345 on Thermal Hyperalgesia and IL-1β mRNA Expression in Inflammatory Tissue of Monoarthritis Rats

目的观察拮抗外周NK-1受体后对关节炎大鼠痛行为和IL-1 β mRNA表达的影响情况,并探讨其可能机制。方法制备大鼠单发局限性佐剂关节炎模型,并检测多次皮下注射不同剂量CP-96345(NK-1受体拮抗剂)后对其热痛阈值和IL-1 β mRNA表达的影响情况。结果皮下注射0．01 M CP-96345可提高关节炎大鼠的热痛阈值,且可抑制CFA 组大鼠IL-1 β mRNA的表达增加(P<0．01)。结论 NK-1受体拮抗剂可抑制关节炎大鼠的痛觉过敏和IL-1 β mRNA的表达,其作用有可能是通过IL-1 β阳性神经细胞上的NK-1受体这一潜在作用靶点起作用。

Objective To observe the effect of a high-affinity, non-peptide antagonist of the NK-1 receptor, CP 96345 on thermal hyperalgesia and IL-1β mRNA expression in inflammatory tissue of monoarthritis rats. Methods Monoarthritis was induced in rats by unilateral injection of complete Freund＇s adjuvant （CFA）.Thermal hyperalgesia was tested by paw withdrawal response to a heat stimulus.And IL-1β mRNA expression was assessed by RT-PCR. Results Subcutaneously injected 0.01 M NK-1 receptor antagonist CP96345 inhibits CFA produced thermal hyperalgesia.0.01M NK-1 receptor antagonist inhibited the IL-1β mRNA expression produced by CFA.Conclusion NK-I receptor on IL-1β positive cells in the inflammatory skin tissue could be potential targets of NK-I receptor antagonist, which may partially underlie NK- 1 receptor antagonist suppressing thermal hyperalgesia and IL- 1β mRNA expression in inflammatory tissue of monoarthritis rats.