血管性痴呆大鼠星形胶质细胞增生与TNF-α的表达

Astrocyte proliferation and expression of TNF-α on vascular dementia in rats

目的 研究星形胶质细胞在血管性痴呆中的反应及特点,探讨炎症反应和血管性痴呆的关系。方法 采用Morris智能水迷宫检测血管性痴呆模型大鼠学习记忆能力的改变情况。采用免疫组化法观察胶质原纤维酸性蛋白(glialfibrillary acidic protein,GFAP)和TNF-α在前脑皮层的表达,高倍镜下观察GFAP标记的星形胶质细胞的形态变化。结果 GFAP在血管性痴呆模型大鼠的前脑皮层表达明显,和对照组比较,差异有显著性(P<0.05),模型组大鼠GFAP标记的星形胶质细胞可见细胞肿胀,突起变粗,分支减少。TNF-α在模型组大鼠的前脑皮层内有较为明显的表达,表达主要集中于皮层外侧,而在对照组几乎不表达。结论 血管性痴呆的病理机制中涉及星形胶质细胞的增殖和形态改变,可能影响了血脑屏障的功能;早期炎症因子的参与可能是继发性损伤的原因之一。

Objective To study the reaction and morphology of astrocytes during vascular dementia and to investigate an association between inflammation and vascular dementia. Methods The ability of rats in learning and memory was tested using Morris water maze. The expressions of glial fibrillary acidic protein (GFAP) and TNF-α in forebrain cortex were observed immunohistochemically and the form of astrocytes marked by GFAP under a light microcopy. Results The expression of GFAP at forebrain cortex in model rats was more remarkable than that in controls (P<0.05). The astrocytes marked by GFAP of model rats got swollen, enlarged and decreased in the number of branches. The expression of TNF-α was significant in forebrain cortex of model rats, mainly on the lateral cortex, while little expression was observed in controls. Conclusion Pathological mechanism of vascular dementia involves proliferation and morphological changes of astrocytes, which may affect function of blood brain barrier. Early inflammation factor may induce the secondary injury.