摘要
目的观察大鼠脑缺血再灌注损伤后脑组织中细胞间黏附分子-1(ICAM-1)和血管间黏附分子-1(VCAM-1)的表达及瑞舒伐他汀干预对其影响。方法 SD大鼠随机分为3组:假手术组(sham组)、模型组(model组)和治疗组(test组)。治疗组在模型制作前用5 mg/(kg·d)瑞舒伐他汀连续灌胃10 d,1次/d。制作大鼠脑缺血再灌注损伤模型,缺血2 h再灌注24 h后,应用免疫组化法、RT-PCR法和Western blot法检测脑组织中ICAM-1和VCAM-1的表达。结果脑缺血再灌注损伤后,脑组织中ICAM-1和VCAM-1的表达明显增加,与假手术组相比有统计学意义(P<0.05);瑞舒伐他汀干预后,能够显著降低脑组织中ICAM-1和VCAM-1的表达,与模型组相比有统计学意义(P<0.05)。结论瑞舒伐他汀可抑制大鼠脑缺血再灌注损伤后脑组织中ICAM-1和VCAM-1的表达。
This study performed to explore the expression of intercellular adhesion molecule-1（ICAM-1） andvascular adhesion molecule-1（VCAM-1）in rats with focal cerebral ischemia-reperfusion and observe interveningeffect of rosuvastatin on their expression. SD rats were randomly assigned into three groups： sham operation group（sham group）, focal cerebral ischemia-reperfusion group（model group） and rosuvastatin preconditioning group（testgroup）. The rats in the test group were lavaged with rosuvastatin of 5 mg/（kg·d） before the model construction. Themiddle cerebral artery occlusion reperfusion model was made by the suture method（ischemia for 2 hours, andreperfusion for 24 hours）. Immunohistochemistry, RT-PCR and Western blot were used to detect the levels ofICAM-1 and VCAM-1. Compared with sham group, the expression levels of ICAM-1 and VCAM-1 weresignificantly up-regulated in rats of model group（P〈0.05）; compared with model group, the expression levels ofICAM-1 and VCAM-1 were significantly down-regulated in rats of test group（P〈0.05）. The result indicated thatrosuvastatin preconditioning can suppress the expression of ICAM-1 and VCAM-1 in rats with focal cerebralischemia-reperfusion.
出处
《免疫学杂志》
CAS
CSCD
北大核心
2016年第1期56-59,共4页
Immunological Journal
基金
福建省教育厅B类课题(JB13303)
泉州市科技计划(2012Z78)
2014年泉州市卫生科研资助
