摘要
目的研究一氧化氮合酶抑制剂对宫内窘迫胎鼠幼年学习记忆能力、海马突触素的影响。方法（1）建立胎鼠宫内窘迫模型；（2）分为正常组（Nor）、缺血再灌注组（t／R）、治疗组（NOSI）。缺血前1．5h注射左旋硝基精氨酸（L—NNA），然后于术前即刻腹腔内注射氨基胍（AG）500mg／kg，将正常组、缺血再灌注组和治疗组中的胎鼠继续妊娠至孕19d，以剖宫产娩出，饲养至40d）；（3）以Morris水迷宫检测幼鼠学习能力后检测海马中突触素的表达情况。结果各组幼鼠历时5d训练，共8个时间段；与Nor、NOSI组比较，I／R组平均潜伏期延长（P〈0．05）。NOSI组与Nor组比较，潜伏期延长，但差异无统计学意义（P〉0．05）；幼鼠在第5天进行的跨平台次数，I／R组较Nor组、NOSI组明显减少（P〈0．05）；而NOSI组与Nor组比较，差异无统计学意义（P〉0．05）。突触素（Syp）的表达：3组的海马均有阳性产物产生，I／R组的COD值较正常组及NOSI组的COD值高，差异有统计学意义（P〈0．05）；正常组与NOSI组的COD值差异无统计学意义（P〉0．05）。结论宫内窘迫对胎鼠脑组织可能造成长期的影响；在宫内窘迫时及时予以NOSI，可能会减轻胎鼠脑损害，改善仔鼠的智能。
Objective To investigate whether intrauterine hypoxia and ischemia can produce long-time effects or NOSI can prevent these damages. Methods Fetal rat intrauterine distress model was constructed. The rats were divided into the normal group, hypoxia and ischemia reperfusion group and treatment group. Pups were given to surrogate mothers and the ability of learning and memory at 40 day of age after delivery were examined. Then the water maze test was performed to detect the space learning ability and memory function of rats, and the changing of synaptophysin levels in hippocampus were detected by immunohistochemical staining. Result Behavioral results show that fetal distress produces cognitive impairment demonstrated by Morris water maze performance including a higher escape latency score and a decreased cross platform time. The COD of Syp positive immunoreactive product in hippocampus were less decreased than that in the normal group or NOSI group. But the behavioral results and the COD of synaptophysin had no difference between normal group and NOSI group. Conclusions Fetal distress produced cognitive impairment and led to the decreasing of synaptophysin in hippocampus. Effective measure can relieve these damages.
出处
《中国医师杂志》
CAS
2009年第2期210-213,共4页
Journal of Chinese Physician
