Cheng Yu-hua, Wang Wei-dong, Sun Li-sha, Cheng Zu-jue, Xu Jiang-ping
Department of Neurosurgery, Jiangxi Headquater Hospital of Chinese People's Armed Police Forces, Nanchang 330001, China.
Di Yi Jun Yi Da Xue Xue Bao. 2003 Oct;23(10):1074-7.
To investigate the effects of selective nitric oxide synthase (NOS) inhibitors on dentate gyrus (DG) neurogenesis after diffuse brain injury (DBI) in adult rats.
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 Aminoguanidine) groups and the corresponding control groups at various time points after DBI.
Intraperitoneal administration 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).
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.
探讨选择性一氧化氮合酶（NOS）抑制剂对成年大鼠弥漫性脑损伤（DBI）后齿状回（DG）神经发生的影响。
在成年雄性SD大鼠中建立DBI模型，随后对分裂细胞进行全身溴脱氧尿苷（BrdU）标记，并对DG中神经前体细胞的增殖率进行免疫组织化学检测，以比较DBI后不同时间点NOS抑制剂（7-硝基吲唑和氨基胍）组与相应对照组的情况。
腹腔注射7-硝基吲唑可显著降低成年大鼠DBI后2、4和6天DG中BrdU标记细胞的数量（P<0.05）。氨基胍在各个时间点也显著抑制DBI诱导的DG中神经前体细胞的增殖（P<0.01）。
DBI后NOS的激活可能是成年大鼠DG神经发生的重要调节因子，nNOS产生的NO可能主要参与DBI后神经发生增强的早期阶段，而iNOS产生的NO可能主要参与后期阶段。
