大鼠脑损伤后氨基胍的神经保护作用  

NEUROPROTECTION WITH AMINOGUANIDINE TREATMENT AFTER BRAIN INJURY IN RATS

作　　者：倪衡建[1] 何志贤[1] 张志军[1] 杨学峰[1] 胡燕[1] 

机构地区：[1]南通大学基础医学院人体解剖学教研室,南通226001

出　　处：《解剖学报》2005年第4期346-350,共5页Acta Anatomica Sinica

基　　金：南通大学中青年科研基金资助项目

摘　　要：目的探讨大鼠脑损伤后诱导性一氧化氮合酶(iNOS)抑制剂———氨基胍(AG)的神经保护作用。方法采用大鼠额叶锐器损伤模型,将SD大鼠随机分成氨基胍(AG)治疗组和生理盐水(NS)对照组。用生物化学方法检测NO含量;RT-PCR法及免疫组织化学染色方法观察iNOSmRNA和iNOS阳性细胞表达变化;末端脱氧核苷酸转移酶介导的原位缺口末端标记法(TUNEL)检测细胞凋亡。将两组结果进行比较。结果AG治疗组创伤区及周边NO含量、iNOSmRNA和iNOS阳性细胞表达量较NS组明显降低,凋亡细胞数量也相应明显减少。结论AG能选择性地抑制iNOS表达,减少NO过量产生,从而减少细胞凋亡,发挥神经保护作用。Objective To investigate the neuroproteetive effect of inducible nitric oxide synthase （iNOS）inhibitor, aminoguanidlne（AG） ,after brain injury in rats. Methods Using frontal sharp cortex injury model,SD rats were randomly divided into AG treat group and NS control group. Biochemical assay, RT-PCR,immunohistochemistry and TUNEL method were used to determine NO content, iNOSmRNA, iNOS positive cells and apoptotic cells respectively. The experimental results were compared in the two groups. Results NO content and the expression of iNOSmRNA and iNOS positive cells in traumatized cortex decreased significantly in AG treat group than that in NS control group. The number of apoptotic cells also reduced correspondently in AG treat group. Conclusion AG could selectively inhibit the expression of iNOS,then reduce NO content,thus reduce apoptotic cells and produce protective effect on cells in injuryed area.

关 键 词：额叶损伤 氨基胍 神经保护 诱导性一氧化氮合酶 末端脱氧核苷酸转移酶介导的原位缺口末端标记法(TUNEL) 逆转录聚合酶连反应 免疫组织化学 大鼠 

分 类 号：R651.1[医药卫生—外科学]