摘要
目的 :探讨环孢素A对大鼠创伤性脑损伤后NO的影响及其可能的作用机制。方法 :取 4 8只Wistar大鼠随机分为A、B、C 3组 ,依次为假创伤组、脑创伤生理盐水治疗组及脑创伤环孢素A(CsA)治疗组。脑创伤模型采用自由落体打击装置建立 ,透射电镜观察脑组织形态学变化 ,Griess法检测各组伤后 2 4h、4 8h脑组织及血清中NO含量变化。结果 :脑组织与血清中NO含量变化趋势极其类似。B组伤后 2 4h、4 8h脑组织NO含量为 (2 97.83±6 .2 8) μmol/g及 (381.4 0± 7.12 ) μmol/g ,较A组对应时间点NO含量明显升高 ,而经CsA治疗的C组分别为(2 30 2 7± 6 0 4 ) μmol/g、(30 0 .4 2± 6 .6 1) μmol/g并伴超微结构的显著改善。结论 :环孢素A能够有效抑制NO在脑组织及血清中的表达 ,其发挥脑保护作用可能与减少NO的生成有关。
Aim:To investigate the effect and mechanism of cyclosporin A (CsA) on nitric oxide (NO) after traumatic brain injury (TBI) in rats.Methods:A total of 48 adult healthy Wistar rats were randomly allocated into 3 groups of 16 each Group A: the sham operation control; group B: underwent brain injury and treated with normal saline; group C:underwent brain injury and treated with CsA. The traumatic brain injury model was established by applying a free falling device hitting the rats' heads directly Histopathological changes were observed under transmission electron microscope. NO contents in brain tissue and serum were tested via Griess methods at 24 h and 48 h after injury.Results:The changing trend of NO content in brain tissues was extremely similar to serum.NO levels in brain tissue at 24 h and 48 h for group B were (297 83±6 28) μmol/g and (381 40±7 12) μmol/g respectively,which were significantly higher than those for group A However,its levels at 24 h and 48 h were (230 27±6 04) μmol/g and (300 42±6 61) μmol/g after treatment with CsA The ultrastructure was also greatly improved.Conclusion:CsA can effectively inhibit the produce of NO in brain tissues and serum The effects of neuroprotection may due to the reduction of NO .
出处
《郑州大学学报（医学版）》
CAS
北大核心
2002年第2期192-194,共3页
Journal of Zhengzhou University(Medical Sciences)
