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目的探讨巨噬细胞游走抑制因子(MIF)在复杂区域疼痛综合征1型(CRPS1)的表达及MIF靶向阻断对CRPS1大鼠疼痛行为的影响。方法健康成年雄性SD大鼠50只,随机分为正常组、假手术组、模型组、治疗对照组及MIF抑制剂(ISO-1)治疗组。后3组均进行CRPS1远端胫骨骨折造模;ISO-1治疗组在骨折2周后开始将ISO-1溶解于10μl5%DMSO后行皮下注射,1mg/(kg.d),连续14d;治疗对照组同期皮下注射10μl 5%DMSO作为对照。测定各组大鼠治疗前后下肢肿胀程度及痛觉阈值并进行比较;采用ELISA、蛋白质印迹法测定各组大鼠血清、脑脊液、皮肤、坐骨神经和脊髓中MIF蛋白的表达并进行比较。结果模型组大鼠后足明显肿胀,疼痛阈值明显下降,与基线值及对照组比较,差异有统计学意义(P<0.01)。MIF抑制剂ISO-1治疗组的下肢肿胀及痛觉阈值均有改善,与模型组相比较,差异有统计学意义(P<0.05)。模型组、治疗对照组及MIF抑制剂(ISO-1)治疗组的MIF在血清、脑脊液、皮肤、坐骨神经和脊髓的表达均高于正常对照组,差异有统计学意义(P<0.05或P<0.01)。结论 MIF是CRPS1的关键性炎症因子,抗MIF可能成为其新的靶向治疗手段。
Objective To investigate the expression of macrophage migration inhibitory factor (MIF) in complex regional pain syndrome type 1 (CRPS1) and the effect of targeted blockade of MIF on pain behavior in CRPS1 rats. Methods Fifty healthy adult male Sprague-Dawley rats were randomly divided into normal group, sham operation group, model group, treatment control group and MIF inhibitor (ISO-1) treatment group. After 3 weeks, the ISO-1 treatment group began to subcutaneous injection of ISO-1 in 10μl 5% DMSO subcutaneously at 1mg / (kg · d) for 14 days. The treatment group In the control group, 10 μl of 5% DMSO was injected subcutaneously as a control. The degree of swelling and the pain threshold of the lower extremities before and after treatment were measured and compared. The expression of MIF protein in serum, cerebrospinal fluid, skin, sciatic nerve and spinal cord of each group was measured by ELISA and Western blot. Results In the model group, the hind paw was obviously swollen and the pain threshold was significantly decreased. Compared with the baseline value and the control group, the difference was statistically significant (P <0.01). MIF inhibitor ISO-1 treatment group lower limb swelling and pain threshold were improved, compared with the model group, the difference was statistically significant (P <0.05). MIF expression in serum, cerebrospinal fluid, skin, sciatic nerve and spinal cord of model group, treatment control group and MIF inhibitor (ISO-1) treatment group were significantly higher than those of normal control group (P <0.05 or P < 0.01). Conclusion MIF is a key inflammatory factor of CRPS1, anti-MIF may be its new target therapy.