摘要
目的 观察NO前体及选择性NOS干预剂对弥漫性脑损伤后齿状回神经发生的调控作用 ,探讨NOS -NO通路在成年脑神经发生中的角色。方法 选用成年弥漫性脑损伤大鼠模型 ,采用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、12d时各干预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 L -精氨酸 (L -Arg) 2 0 0mg/kgi.p .后 ,成年大鼠弥漫性脑损伤后各个时间点海马齿状回BrdU免疫阳性细胞数目均显著增多 ,以脑损伤后 6d和 8d时增加最为明显 (P <0 0 1)。 7-硝基引唑 (7-NI) 5 0mg/kgi.p .后 ,明显抑制了大鼠弥漫性脑损伤后不同时间点齿状回细胞增殖 ,在弥漫性脑损伤后 4d时抑制作用相对最为明显 (P <0 0 1)。氨基胍 (AG) 10 0mg/kgi.p .后 ,也明显减少了大鼠弥漫性脑损伤后不同时间点齿状回BrdU免疫阳性细胞数目 ,从第 8天后抑制作用相对更为明显 (P <0 0 1)。结论 弥漫性脑损伤后激活的NOS -NO通路是海马齿状回神经发生过程中一个重要的调控通路 ,不同来源的NO分别在弥漫性脑损伤后不同时间齿状回神经发生中发挥作用。
Objective To investigate the effects of NO donor and selective NOS inhibitors on dentate granule cell neurogenesis after diffuse brain injury(DBI) in the adult rat, and to discuss the role of NO in neurogenesis after DBI.Methods Adult male SD rats were subjected to diffuse brain injury model. Using systemic bromodeoxy-uridine (BrdU) to label dividing cells, we compared the proliferation rate of neural precursor cells in the dentate gyrus between intervention group and corresponding control group at various time points after diffuse brain injury. Results After L-Arg (20 mg/kg i.p.) injection, the number of BrdU labeled cells in the dentate gyrus after diffuse brain injury significantly increased at various time points and there was a prominent enhancement on the cell proliferation at the 6th and 8th day (P<0.01). 7-NI was injected (50 mg/kg i.p.) significantly reduced the number of BrdU labeled cells in the dentate gyrus at various time points after DBI with a prominent inhibition of the cell proliferation at the 4th day (P<0.01). Aminoguanidine (100 mg/kg i.p.) also significantly inhibited the proliferation rate of neural precursor cells in the dentate gyrus at various time points after DBI, but its obvious inhibition presented at the 8 day (P<0.01).Conclusion The activation of NOS-NO pathway after DBI maybe promote the neurogenesis in the dentate gyrus. The NO coming from nNOS was probably mainly involved in the early enhanced neurogenesis after DBI, while the NO originating from iNOS probably participated in the late enhanced neurogenesis primarily.
出处
《中国急救医学》
CAS
CSCD
北大核心
2004年第1期25-27,共3页
Chinese Journal of Critical Care Medicine
基金
国家 8 63计划资助项目 (No .2 0 0 3AA2Z3 5 3 5 )
