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TIO对LPS诱导脑内炎症反应中血脑屏障的保护作用
引用本文:朱耀峰,张剑峰,卢璨,周奕,雷德亮. TIO对LPS诱导脑内炎症反应中血脑屏障的保护作用[J]. 生物磁学, 2012, 0(33): 6405-6407,6404
作者姓名:朱耀峰  张剑峰  卢璨  周奕  雷德亮
作者单位:[1]中南大学基础医学院人体解剖与神经生物系,湖南长沙410013 [2]吉首大学医学院人体解剖教研室,湖南吉首416000 [3]中南大学湘雅医学院,湖南长沙410013 [4]长沙医学高等专科学校解剖教研室,湖南长沙410013
基金项目:中南大学2010年度米塔尔学生创新项目(10MX19)
摘    要:目的:研究雷公藤甲素对内毒素诱导的脑内炎症中血脑屏障通透性,神经细胞的保护作用。方法:选用健康成年雄性SD大鼠,随机分为雷公藤甲素处理组(T10+LPS组),内毒素组(LPs组),生理盐水组(NS组),每组6只动物常规Nissl染色、GFAP免疫组化染色和伊文思蓝(EB)荧光示踪法。结果:尼氏染色显示NS组海马CAl区锥体神经元排列规则整齐。LPS组的神经元细胞的密度和层次较NS组和T10+LPS组少,且锥体神经元数目减少,排列散乱,细胞间距加大,神经元有明显的丢失;GFAP免疫组化染色结果显示,NS组海马CAl区GFAP免疫阳性细胞分布稀疏,胞体较小,突起细长,染色较浅。LPS组较T10+LPS组星形胶质细胞密集,胞体和突起大,染色深;伊文思蓝荧光示踪结果,LPS组的大脑皮质与海马结构以及脑血管周围的EB荧光强度都明显强于T10+LPS组和NS组;T10+LPS组与NS组EB荧光强度无差别。结论:T10在LPS诱导的神经炎症中对神经元有保护作用,其机制可能与保护BBB有关。

关 键 词:雷公藤甲素  内毒素  血脑屏障

The Protective Effects of Triptolide on Blood Brain Barrier in Cerebral Inflammation Induced by LPS
ZHU Yao-fen,ZHANG Jian-feng,LU Can,ZHOU Yi,LEI De-liang. The Protective Effects of Triptolide on Blood Brain Barrier in Cerebral Inflammation Induced by LPS[J]. Biomagnetism, 2012, 0(33): 6405-6407,6404
Authors:ZHU Yao-fen  ZHANG Jian-feng  LU Can  ZHOU Yi  LEI De-liang
Affiliation:1 Department of The Human Anatomy and Neurobiologic Xiangya School oMedicine, Central South University, Changsha I-Iunan, 410013 ,China; 2 Department of The Human Anatomy, Jishou University, Jishou, Hunan,416000, China; 3 Xiangya School of Medicine, Central South University, Changsha Hunan, 410013, China; 4 Department of The Human Anatomy of Changsha medical college, Changsha Hunan, 410013, China)
Abstract:Objective: To investigate the effects of triptolide on the permeability of blood brain barrier and protection of neurocytes during cerebral inflammation induced by LPS. Methods: Healthy adult male SD rats were divided into 3 groups: triptolide group (T10+LPS), LPS group, NS group, with 6 rats in each group. Regular Nissl's staing,GFAP immunohistochemical staing and Evans blue fluorescence tracer method were used in the present study. Results: The results of Nissl's staining showed that in NS group, the pyramidal cells in the hippocampal CA1 region arranged regularly and the loss of neurons was unremarkable. In LPS group, either the density or the layers of both neurons and pyramidal cells was less than that in (T10+LPS) group or NS group. Neurocytes of the rats in LPS group scattered randomly and the intercellular spaces increased. For immunohistochemical staining of GFAP, it revealed that the staining positive cells distributed sparsely in the hippoeampal CA1 region of the rats in NS group, which had smaller cell bodies and slender processes, and also were stained more lightly. Both the number and color depth of the positive cells increased more obviously in LPS group or (T10+LPS) group compared to that in NS group. The number of astrocytes increased, the cell bodies and processes were bigger, and the color of the stained cells was darker in LPS group than those in (T10+LPS) group. In the analysis of Evans blue fluorescence staining, the intensity of EB fluorescence in cerebral cortex and hippocampus formation, and around the cerebral vessels was higher than that in (T10 +LPS) group or NS group. However, there was no significant difference between the results of EB fluorescence staining of(T10+LPS) group and NS group. Conclusion: The study suggests that T10 may influence the function of BBB and reduced the inflammation reaction of astrocytes to protect the neurocytes from impairment during cerebral inflammation process induced by LPS.
Keywords:T10  LPS  Blood Brain Barrier
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