Expression of Claudin-5 and ZO-1 in Early Brain Injury after Subarachnoid Hemorrhage in Rats
- VernacularTitle:紧密连接相关蛋白Claudin-5、ZO-1在大鼠蛛网膜下腔出血后早期脑损伤中的表达及意义
- Author:
Duo CHEN
;
Jiangwei YUAN
;
I_ei SONG
;
Xiangtai WEI
;
Junhong GUAN
;
Yunhui LIU
;
Zhihong ZONG
- Publication Type:Journal Article
- Keywords:
subarachnoid hemorrhage;
early brain injury;
tight junction protein;
blood-braln barrier;
rat
- From:
Journal of China Medical University
2010;(9):713-716
- CountryChina
- Language:Chinese
-
Abstract:
Objective Aimed to clarify the molecular mechanism after subarachnoid hemorrhage （SAH） by investigating the expression of tight junction protein Claudin-5 and ZO-1 and the effects of SP600125 on them. Methods Seventy-five male Sprague Dawley rats （300 to 350 g） were randomly divided into sham,SAH,SAH ＋ DMSO （dimethyl sufoxide） solution,SAH ＋SP600125 （C-Jun N-terminal kinase inhibitor）10 mg/kg,and SAH ＋SP600125 30 mg/kg groups. The standard endovaseular perforation was performed to produce experimental SAH. The JNK inhibitor SP600125 was intraperitoneally administered at 1 hour before and 6 hours after SAH. Results At 24 hours after SAH,signs of microvessels injury were observed in brain cortex. Compared with the sham group,expression of Claudin-5 and ZO-1 was sig- nificantly decreased （P 〈 0.05 ）. JNK inhibitior SP600125 suppressed the decrease of Claudin-5 and ZO-1 expression, attenuated blood-brain barrier disruption in rats after SAH. Conclusions The blood-brain barrier disruption is an important mechanism of early brain injury after SAH. JNK inhibitor SP600125 improves neurological outcomes and provides neuropmtecfion against acute events after SAH such as bloodbrain barrier disruption and cell apoptosis.
