NOS抑制剂对成年大鼠弥漫性脑损伤后海马齿状回神经发生的影响  

Effects of nitric oxide synthase inhibitor on dentate gyrus neurogenesis after diffuse brain injury in adult rats

作　　者：程毓华[1] 王卫东[2] 孙莉莎[1] 程祖珏[1] 徐江平[2] 

机构地区：[1]武警江西总队医院神经外科,江西南昌330001510515 [2]第一军医大学药理教研室,广东广州510515

出　　处：《第一军医大学学报》2003年第10期1074-1077,共4页Journal of First Military Medical University

摘　　要：目的观察一氧化氮合酶(NOS)抑制剂对成年大鼠弥漫性脑损伤后齿状回神经发生的影响。方法建立成年弥漫性脑损伤(DBI)大鼠模型,采用5-溴脱氧尿核苷(BrdU)标记分裂细胞及免疫组织化学方法比较弥漫性脑损伤后2、4、6、8、12 d时NOS抑制剂干预组大鼠与相应对照组大鼠之间海马齿状回神经前体细胞的增殖速度。结果成年大鼠弥漫性脑损伤后应用7-硝基引唑(7-NI) 进行干预可抑制脑损伤后第2、4、6天时齿状回神经前体细胞的增殖(P<0.05)。应用氨基胍进行干预可明显减少大鼠弥漫性脑损伤诱导的各个时间点齿状回BrdU免疫阳性细胞数目(P<0.01)。结论NOS可能是弥漫性脑损伤后成年大鼠海马齿状回神经发生过程中一个重要的调节因子,不同类型的NOS在弥漫性脑损伤后神经发生过程中的不同阶段可能扮演了不同的角色。Objective To investigate the effects of selective nitric oxide synthase (NOS) inhibitors on dentate gyrus (DG) neurogenesis after diffuse brain injury (DBI) in adult rats. Methods DBI models were established in adult male SD rats, followed by systemic bromodeoxyuridine (BrdU) labeling of the dividing cells and immunohistochemical assay of the proliferation rates of neural precursor cells in the DG for comparison between NOS inhibitor (7-nitroindazole and Amino- guanidine) groups and the corresponding control groups at various time points after DBI. Results Intraperitoneal admini- stration of 7-nitroindazole significantly reduced the number of BrdU-labeled cells in the DG of adult rats 2, 4 and 6 d after DBI (P<0.05). Aminoguanidine also significantly inhibited the proliferation of neural precursor cells in the DG induced by DBI at various time points (P<0.01). Conclusions The activation of NOS after DBI may be an important regulatory factor for DG neurogenesis in adult rats, and NO generated by nNOS is probably involved mainly in the early stage of enhanced neurogenesis after DBI, while the NO from iNOS might participated primarily in the later stages.

关 键 词：NOS抑制剂 成年大鼠 弥漫性脑损伤 海马齿状回神经 一氧化氮合酶抑制剂 

分 类 号：R651.1[医药卫生—外科学]