IP-10和JNK介导CFA诱导的大鼠足底炎性疼痛
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The mediation of IP-10 and JNK on CFA-induced inflammatory pain in the rat’s paw
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    摘要:

    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CFA 150 μl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3 h-6 h-1天,在注射部位足底皮肤IP-10 mRNA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-

    Abstract:

    Objective:To examine CFA(complete Freund’s adjuvant)-induced IP-10 expression in the paw skin and the regulation of c-jun N-terminal kinase(JNK) inhibitor on CFA-induced pain and IP-10 expression. Methods:CFA was injected into the rat’s unilateral hind paw to induce chronic inflammatory pain. Heat hyperalgesia on both hind paws were tested at different time points after injection of CFA. Reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) were used to examine the expression of IP-10 mRNA and protein in the paw skin respectively. By intraplantar injection,the effect of JNK inhibitor SP600125 on CFA-induced pain and IP-10 upregulation was detected. Results:Peripheral injection of CFA induced persistent heat hyperalgesia. Both IP-10 mRNA and protein expression were increased in the paw skin at the time points of 3 h,6 h and 1 d after CFA injection. Intraplantar injection of SP600125 attenuated CFA-induced heat hyperalgesia and reduced IP-10 expression. Conclusion:IP-10 is involved in CFA-induced pain. JNK plays a role in pain and IP-10 expression induced by CFA.

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朱鸣镝,钱丽玲,朱〓俐,高永静. IP-10和JNK介导CFA诱导的大鼠足底炎性疼痛[J].南京医科大学学报(自然科学版),2009,29(12):1698-1702

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  • 收稿日期:2009-09-11
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