文章摘要
钙调神经磷酸酶在弗氏佐剂致大鼠炎性痛中的作用
Calcineurin in inflammatory pain induced by Complete Freund′s adjuvant in rats
  
DOI：
中文关键词: 钙调神经磷酸酶  核因子κB  IL-10  炎性痛
英文关键词: Calcineurin  Nuclear factor kappa B  Interleukin-10  Inflammation pain
基金项目:内蒙古自治区自然科学基金（2014MS0882）
作者单位
王爱桃 010017,呼和浩特市,内蒙古自治区人民医院麻醉科 
姚尚龙 华中科技大学附属武汉协和医院 
杜晓冰 010017,呼和浩特市,内蒙古自治区人民医院麻醉科 
王丹 内蒙古医科大学研究生院 
董海云 内蒙古医科大学研究生院 
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中文摘要:
      目的 探讨钙调神经磷酸酶（calcineurin,CaN）在弗氏佐剂致大鼠炎性痛痛觉过敏中的作用。方法 选择雄性SD大鼠75只,体重200～300 g,将其随机均分为对照组(C组)、完全弗氏佐剂(CFA)组(F组)和CaN+CFA组(NF组)。C组大鼠右侧后爪趾底注射生理盐水100 μl,F组和NF组大鼠右侧后爪趾底注射CFA 100 μl制备炎性痛模型,NF组大鼠于右侧后爪趾底注射CFA前1 d鞘内注射CaN 10 U。三组大鼠于右侧后爪趾底注射前30 min (T0)、注射后05 h (T1)、1 h (T2)、2 h (T3) 及4 h (T4) 测定大鼠热刺激缩足潜伏期(PWTL);同时各取5只大鼠脊髓组织,Western blot法测定各组大鼠脊髓中CaN、核因子κB(NF-κB)p65蛋白含量;RT-PCR法测定大鼠脊髓中CaN及NF-κB基因的表达。ELISA法测定大鼠脊髓组织中IL-1β、TNF-α和IL-10浓度。结果 T2～T4时F组, T3、T4时NF组 PWTL明显短于T0时和C组(P＜0.05);T2～T4时NF组PWTL明显长于F组(P＜0.05)。T1～T4时F组,T2～T4时NF组脊髓组织CaN蛋白含量明显低于,NF-κB p65蛋白明显高于T0时和C组(P＜0.05)；T2～T4时F组、NF组脊髓组织CaN基因表达、IL-10浓度明显低于，NF-κB基因表达及IL-1β、TNF-α浓度明显高于T0时和C组（P＜0.05）;T1～T4时NF组脊髓组织CaN蛋白含量和基因表达明显高于,NF-κB p65蛋白含量和基因表达及IL-1β、TNF-α明显低于，IL-10浓度明显高于F组(P＜0.05)。结论 CaN通过抑制NF-κB，调节抗炎细胞因子和促炎细胞因子的平衡，抑制大鼠炎性痛的发生发展。
英文摘要:
      Objective To investigate the role of calcineurin(CaN)in inflammatory pain in rats. Methods Seventy-five male Harlan-Sprague-Dawley rats, weighting of 200-300 g were randomly divided into 3 groups (n=25): group control (group C), group CFA (complete Freunds adjuvant) (group F) and group CaN+CFA (group NF). 100 μl CFA were injected on the right hind claw preparaing for inflammatory pain models in groups F and NF, 100 μl saline were injected on the right hind claw in group C. CaN 10 U was intracerebroventricular injected 1 d before CFA injection in group NF. Paw withdrawal thermal latency (PWTL) were measured in 30 min prior to (T0), 05 h (T1), 1 h (T2), 2 h (T3) and 4 h (T4) after injection. The expression of CaN and nuclear factor kappa B (NF-κB), IL-1β, TNF-α and IL-10 in spinal cord were measured at each time point. Results The PWTL was significantly shorter at T2-T4 in group F, at T3, T4 in group NF than that at T0 and in group C (P＜0.05); The PWTL at T2-T4 in group NF was significantly longer than that in group F (P＜0.05). CaN protein expression in spinal cord at T1-T4 in group F, at T2-T4 in group NF was significantly lower than that of T0 and in the group C, NF-κB p65 protein expression was significantly higher than that of T0 and in the group C (P＜0.05). CaN gene and IL-10 protein content at T2-T4 in groups F and NF were significantly lower than that of group C and at T0, NF-κB gene and IL-1β, TNF-α protein content was significantly higher than that of group C and at T0 (P＜0.05). CaN protein and CaN gene expression, IL-10 protein content in spinal cord tissue at T1-T4 in group NF was significantly higher than that of group F, NF-κB p65 protein and NF-κB gene expression and contents of IL-1β,TNF-α protein were significantly lower than that of group F (P＜0.05). Conclusion CaN adjusts pro inflammatory and anti inflammatory cytokines by reducing NF-κB and inhibiting the process of inflammatory pain in rats.
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