摘要
目的研究丹酚酸B(SalB)对脑缺血再灌注损伤大鼠炎症反应的干预作用。方法雄性Wistar大鼠随机分为3组:假手术组、模型组、实验组,制作脑中动脉闭塞模型(MCAO),缺血1 h再灌注。分别于大鼠苏醒后、再灌注24,48 h,实验组腹腔注射SalB(12 mg·kg-1),模型组以等体积0.9%NaCl替代。在4个时间点(6,24,48,72 h)进行神经功能缺损评分,检测外周血白细胞计数、中性粒细胞绝对值,ELISA法检测血浆C反应蛋白水平(CRP),实时荧光定量RTPCR法检测缺血侧脑组织ICAM-1、E-selectin mRNA表达。结果 SalB可以改善模型大鼠神经功能缺损症状,降低外周血白细胞计数、中性粒细胞绝对值及血浆CRP水平,抑制缺血侧脑组织ICAM-1、E-selectin mRNA表达。结论SalB具有抗脑缺血再灌注损伤作用,其机制可能与抑制损伤后整体炎症反应水平及脑组织内黏附分子的表达有关。
Objective To research interventional effect of salvianolic acid B （ SalB） on inflammatory reaction after cerebral ischemia reperfu-sion injury.Methods Wistar rats were randomly divided into sham operation group, model group and experiment groups.Rat Ischemia -reperfusion injury model was established by ischemia 1 h and reperfu-sion.SalB （ 12 mg · kg -1 , experiment group ） or 0.9%NaCl （ model group） were administered intraperitoneally while rats were awake from surgery and 24 h, 48 h after reperfusion.At 4 time points （6, 24, 48, 72 h after reperfusion ） , the neurological deficit scores were evaluated , while automatic blood cell analyzer detection for peripheral blood white blood cell , absolute neutrophil count .ELISA method was used to detect plasma C-reactive protein （ CRP ） levels.The real -time fluorescence quantitative RT -PCR was used to detect cerebra tissue ICAM -1, E-selectin mRNA expression.Results SalB could improve middle cer-ebral artery occlusion （ MCAO） rat neurological function and reduce the brain damage , decrease the peripheral blood white blood cell , absolute neutrophil count , plasma CRP, depress adhesion molecules including ICAM-1 , E-selectin mRNA expression in cerebral tissue.Conclusion SalB has anti -cerebral ischemia reperfusion injury effect and the mechanisms were related to overall inflammatory responses and expressionof adhesion molecules after cerebral injury.
出处
《中国临床药理学杂志》
CAS
CSCD
北大核心
2014年第8期704-707,共4页
The Chinese Journal of Clinical Pharmacology
基金
国家自然科学基金资助项目(30801499)
天津市应用基础与前沿技术研究计划基金资助项目(13JCZDJC31500)
关键词
丹酚酸B
脑缺血
再灌注损伤
炎症反应
黏附分子
salvianolic acid B
brain ischemia
reperfusion injury
inflammation
adhesion molecule
