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目的:研究完全弗氏佐剂(CFA)外周注射诱导的趋化因子干扰素诱导蛋白10(IP-10)在局部皮肤的表达,以及JNK激酶抑制剂对CFA诱导的疼痛和IP-10表达的调节。方法:大鼠单侧足底皮下注射CFA150μl诱导大鼠慢性炎症性疼痛。在注射后不同时间点,检测双侧足底的热痛觉过敏。通过逆转录-聚合酶链反应(RT-PCR)、酶联免疫吸附反应试验(ELISA)的方法,分别从mRNA和蛋白水平检测大鼠注射CFA后的足底皮肤中趋化因子IP-10表达的变化。通过在足底注射JNK抑制剂SP600125,观测其对疼痛的产生和IP-10表达的影响。结果:大鼠单侧足底皮下注射CFA诱导足底长时间的热痛觉过敏。在注射后3h、6h、1天,在注射部位足底皮肤IP-10mRNA和蛋白表达均明显增加;足底注射JNK抑制剂,能有效延迟热痛觉过敏的形成和足底皮肤中趋化因子IP-10的表达上调。结论:趋化因子IP-10参与CFA诱导的疼痛,而且JNK激酶能够调控CFA诱导的疼痛和IP-10的表达。
OBJECTIVE: To investigate the expression of interferon-inducible protein 10 (IP-10), a chemokine induced by percutaneous injection of complete Freund’s adjuvant (CFA), on the local skin and the effect of JNK kinase inhibitor on CFA-induced pain and IP-10 expression adjust. Methods: Chronic inflammatory pain was induced by subcutaneous injection of CFA150μl into the unilateral plantar of rats. At various time points after injection, thermal hyperalgesia was examined on both plantar sites. The expression of chemokine IP-10 in the plantar skin after CFA injection in rats was detected by mRNA and protein levels by reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) The change. The effects on pain production and IP-10 expression were observed by injecting SP600125 JNK inhibitor into the plantar. RESULTS: Subcutaneous injection of CFA into the unilateral plantar foot induced prolonged thermal hyperalgesia in the plantar. At 3h, 6h, 1d after injection, the expression of IP-10mRNA and protein in plantar skin increased significantly at the injection site. Plantar injection of JNK inhibitor could delay the formation of thermal hyperalgesia and chemotactic factor IP in plantar skin -10 expression increased. Conclusions: Chemokine IP-10 is involved in CFA-induced pain, and JNK kinase regulates CFA-induced pain and IP-10 expression.