文献类型：期刊文章

作　　者：蔡志友[1] 晏勇[2] 陈然[1]

机构地区：[1]安徽省六安市人民医院神经内科,安徽医科大学第五临床学院 [2]重庆医科大学附属第一医院神经内科,重庆市神经病学重点实验室,六安237005

出　　处：《Neuroscience Bulletin》

基　　金：supported in part by High Technology Research Center, Chongqing Medical University and the Ministry of Civil Affairs,China.

年　　份：2010

卷　　号：26

期　　号：1

起止页码：28-36

语　　种：中文

收录情况：CAS、CSCD、CSCD2011_2012、EBSCO、EMBASE、IC、JST、PUBMED、SCI(收录号：WOS:000295723400004)、SCI-EXPANDED(收录号：WOS:000295723400004)、SCIE、SCOPUS、WOS、ZGKJHX、普通刊

摘　　要：Objective To study the neuroprotective mechanism of minocycline against vascular cognitive impairment after cerebral ischemia. Methods The rat model with vascular cognitive impairment was established by permanent bilateral common carotid artery occlusion （BCCAO）. The observing time-points were determined at 4, 8 and 16 weeks after BCCAO. Animals were randomly divided into sham-operated group （n = 6）, model group （subdivided into 3 groups： 4 weeks after BCCAO, n = 6; 8 weeks after BCCAO, n = 6; and 16 weeks after BCCAO, n = 6）, and minocycline group （subdivided into 3 groups： 4 weeks after BCCAO, n = 6; 8 weeks after BCCAO, n = 6; and 16 weeks after BCCAO, n = 6）. Minocycline was administered by douche via stomach after BCCAO until sacrifice. Glial fibrillary acidic protein （GFAP） was examined by Western blotting and immunohistochemistry. Levels of cyclooxygenase-2 （COX-2） and nuclear factor-kappaB （NF-κB） were measured by immunohistochemistry. IL-1β and TNF-α levels were tested with ELISA method. Results Levels of GFAP, COX- 2, NF-κB, IL-1β and TNF-α were all up-regulated after permanent BCCAO, which could be significantly inhibited by minocycline. Conclusion Minocycline could ameliorate the inflammation and oxidative stress in the hippocampus of the vascular cognitive impairment rat model.

关 键 词：vascular cognitive impairment  MINOCYCLINE INFLAMMATION ASTROCYTE

分 类 号：R749.1]