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目的观察单纯性脑震荡(pure cerebral concussion,PCC)大鼠海马脑区诱导性一氧化氮合酶(inducible nitric oxide synthase,i NOS)的表达变化,探讨i NOS表达变化规律及其与PCC之间的病理联系。方法采用单摆闭合式脑损伤打击装置制造PCC大鼠模型,造模后随机分为3 h、12 h、1 d、2 d、3d、7 d六个损伤组(n=5),另设正常对照组(n=5)。采用i NOS单克隆抗体(鼠)进行免疫组织化学SP法染色和Western Blot实验,检测PCC组和正常组大鼠海马(CA1~4及上、下齿状回)i NOS表达的定位及定量情况。结果正常生理状态下,海马i NOS阳性细胞染色较浅、轮廓不清,且i NOS蛋白表达较弱,致伤后3 h组i NOS阳性表达开始增强,在3 d组出现表达高峰,i NOS蛋白表达高峰出现在2 d组,与正常组比较均有显著性差异(P<0.05),随后均出现下降,至7 d均仍高于正常组。结论 PCC损伤早期海马脑区出现i NOS表达增强,提示i NOS是参与PCC继发性病理损伤的主要炎症因子之一。
Objective To investigate the expression of inducible nitric oxide synthase (iNOS) in the brain of pure cerebral concussion (PCC) rats and to investigate the change of iNOS expression and its relationship with PCC Pathological connection. Methods PCC rat models were made by using a pendulum closed brain injury device and were randomly divided into six injury groups (n = 5) at 3 h, 12 h, 1 d, 2 d, 3d, and 7 d. Normal control group (n = 5). Using iNOS monoclonal antibody (mouse) immunohistochemical SP staining and Western Blot experiments to detect the PCC group and normal hippocampal (CA1 ~ 4 and upper and lower dentate gyrus) i NOS expression and quantitative status . Results Under normal physiological conditions, hippocampus i NOS positive cells stained slightly, with unclear outline, and i NOS protein expression was weak. The i NOS positive expression began to increase 3 h after injury, peaked at 3 d, i NOS The peak of protein expression appeared in the 2 d group, which was significantly lower than that in the normal group (P <0.05), and then decreased at 7 d, which was still higher than that in the normal group. Conclusions The expression of iNOS in the early hippocampus of PCC lesion is increased, suggesting that iNOS is one of the major inflammatory factors involved in the secondary pathological injury of PCC.