补体3干预补体3基因敲除鼠神经病理性疼痛模型的研究

摘要

目的:观察补体3(C3)在神经病理性疼痛模型中的作用.方法:36只C3基因敲除小鼠随机分3组:A组:假手术组;B组:慢性坐骨神经结扎(CCI)模型组;C组:CCI模型干预组.测定小鼠的热痛阈值和机械痛阈值、脊髓SOD活力和MDA的组织含量.结果:与A组相比,B、C组痛阈均明显下降,P<0.05;C组与B组相比,C组痛阈下降幅度更大,差异具有显著性.与A组相比,B组小鼠术后第3、7天脊髓组织SOD活力明显降低而MDA显著升高;C组SOD和MDA变化幅度显著大于B组:C组内第7天与第3天相比,SOD活力增加且MDA含量减少.结论:C3显著增加了补体C3基因敲除小鼠痛敏状态,促进和维持了神经病理性疼痛状态.%Objective: To observe the effects of complement 3 (C3) on neuropathic pain (NPP) in mice.Method: Thirty-six C3-gene knock out mice were divided randomly into 3 groups as following: group A received sham operation; group B received chronic sciatic constriction injury (CCI) operation; group C received CCI operation and C3 lateral ventricles injection postoperation. Pain threshold by thermal and mechanical stimulation were recorded respectively. And the levels of superoxide dismutase (SOD) and malondialdehyde (MDA) in the related segments of spinal cord were detected.Result: Compared with the mice in group A, pain thresholds of paw withdraw postoperation in group B and group C significantly decreased (P＜0.05). Compared with the mice in group B, those in group C showed more magnitude of changing range. Compared with the mice in group A, in group B SOD activity decreased and MDA level increased significantly in spine tissues.The change magnitudes of SOD and MDA in group C were obviously more than those in group B. In group C SOD activity increased and MDA level decreased on the 7th d more than those on the 3rd d.Conclusion: The pain sensitivity increased significantly in CCI models of C3 gene knockout mice by exogenous C3 protein lateral ventricle injection, and it may be contribute to the promoting and maintaining of neuropathic pain.