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目的 : 研究胚胎期和新生期碘缺乏、甲状腺功能低下对大鼠不同脑区 (海马、小脑、大脑皮质 )一氧化氮 (NO)含量的影响。方法 : 复制缺碘大鼠动物模型 ,取子代第 2、3胎大鼠各2 4只分别测定大脑匀浆蛋白质和 NO含量。结果 : 胚胎期和新生期碘缺乏、甲状腺功能低下的子鼠尿碘含量、血清 T3 、T4 含量都较正常对照组明显为低 (P<0 .0 1 ) ,有明显的生长发育障碍 (P<0 .0 1 ) ,学习记忆低下 (P<0 .0 1 )。 子鼠脑 NO含量的测定表明 ,海马 NO含量较正常对照组明显降低 ,差异有显著意义 (1 1 .6 1±2 .3 1 /2 .3 6± 1 .1 8μmol/g prot,P<0 .0 5 )。小脑 NO含量也明显降低 (1 0 .77± 5 .1 6 /4 .70± 1 .95μmol/g Prot,P<0 .0 5 )。大脑皮质 NO含量与对照组比较无明显差异。结论 : 胚胎期和新生期碘缺乏、甲状腺功能低下对子鼠脑组织 NO含量有影响。大脑不同区域对碘缺乏、甲状腺功能低下所致损伤敏感程度不同 ,海马内与 NO有关的代谢异常最明显 ,这一变化可能参与了碘缺乏大鼠学习记忆低下的发病机制。
Objective: To investigate the effects of iodine deficiency and hypothyroidism during embryonic and neonatal period on nitric oxide (NO) content in different brain regions of rats (hippocampus, cerebellum, cerebral cortex). Methods: Animal models of iodine deficient rats were duplicated. The contents of protein and NO in brain homogenates were measured respectively in 24 and 2 rats respectively. Results: The content of urinary iodine and the contents of T3 and T4 in the neonatal rats with hypothyroidism and hypothyroidism during embryonic and neonatal period were significantly lower than those in the normal control group (P <0.01), with obvious growth and development disorders (P <0.01), low learning and memory (P <0.01). The determination of NO content in the rat brain showed that the content of NO in hippocampus was significantly lower than that in the normal control group, with significant difference (1 1 .6 1 ± 2 .3 1/2. 36 ± 1 1 8μmol / g prot, P < 0 .0 5). The content of NO in cerebellum also decreased significantly (100.77 ± 5.16 / 4.70 ± 1.95μmol / g Prot, P <0.05). NO content in cerebral cortex no significant difference compared with the control group. Conclusion: Iodine deficiency in embryonic and neonatal period and hypothyroidism affect the content of NO in brain tissue of offspring rats. Different regions of the brain are sensitive to damage caused by iodine deficiency and hypothyroidism. The metabolic abnormalities related to NO in hippocampus are the most obvious. This change may be involved in the pathogenesis of low learning and memory in iodine deficiency rats.