雷公藤内酯醇对阿尔茨海默病模型大鼠海马突触素表达及突触超微结构的影响

Effects of triptolide on synaptic ultrastructure and synaptophysin expression of hippocampus in model rats with Alzheimer＇s disease

目的：探讨雷公藤内酯醇对阿尔茨海默病模型大鼠海马突触素表达及突触超微结构的影响.方法：大鼠随机分成对照组、模型组、治疗组.模型组给予双侧海马各一次性注射凝聚态Aβ1-4010μg,治疗组在海马注射凝聚态Aβ1-40后,每日腹腔注射雷公藤内酯醇0 4mg/kg, 15d后用免疫组织化学方法和蛋白免疫印迹技术检测海马突触素表达情况,透射电镜观察突触结构的变化.结果：与模型组相比,治疗组海马区突触素免疫反应阳性产物数量（152 80±15 76）及平均光密度（0 3180±0 0278）均增加;突触素表达总量（1917 71±41 02）及密度比值（0 87±0 03）亦增加;突触结构较清晰,界面增长,突触后电子致密物增厚.结论：雷公藤内酯醇可以增加阿尔茨海默病模型大鼠海马突触素的表达,减轻阿尔茨海默病模型大鼠海马突触损伤程度.

Objective：To observe the effects of triptolide （TP） on synaptic ultrastrueture and synaptophysin expression of hippocampus in model rats with Alzheimer＇s disease （AID）. Methods： Rats were randomly derided into a control group, a model group and a treatment group. The model group was given a one-time injection of A[31-40 （10/lg）, the treatment group was given daily intraperitoneal injection of TP （0. 4 mg/kg） after injection of Aβ1-40. 15 days later, the synaptic uhrastructure and synaptophysin expression of hippocampus were observed with transmission electron microscope, immunohistochemistry and Western blot. Results： Compared with the model group, the number （152. 80±15.76） and average optical density （0. 318 0±0. 027 8） of immunoreactive product of synaptophysin increased in the treatment group; the volume （1 917. 71±41.02） and the density ratio （0. 87±0. 03） of synaptophysin expression increased too. Synaptic uhrastructure was more clear, the interface length increased, and the postsynaptic density was thicker. Conclution： TP can increase synaptophysin expression of the hippocarnpus, and reduce the synaptic injury in model rats with AD.