氯沙坦对大鼠局灶性脑缺血再灌注损伤后炎症反应的影响  

Anti-inflammatory effects of losartan on focal brain ischemia/reperfusion injury in rats

作　　者：孙霞[1] 魏欣冰[1] 孙茹[1] 王立祥[1] 李雪梅[1] 张岫美[1] 

机构地区：[1]山东大学医学院药理学研究所,山东济南250012

出　　处：《山东大学学报（医学版）》2005年第11期997-1000,共4页Journal of Shandong University:Health Sciences

摘　　要：目的:观察血管紧张素Ⅱ受体阻断药氯沙坦对大鼠局灶性脑缺血再灌注损伤后炎症反应的影响。方法:采用血管内栓线阻断法制备大鼠局灶性脑缺血再灌注损伤模型,于缺血1h、再灌注24h进行病理组织学检测中性粒细胞浸润、测定髓过氧化物酶(MPO)活性及免疫组化法测定细胞间黏附分子(ICAM-1)的表达。结果:氯沙坦可减少中性粒细胞浸润、降低MPO活性及抑制ICAM-1的表达。结论:氯沙坦通过阻断血管紧张素Ⅱ(AngⅡ)与血管紧张素Ⅱ一型(AT1)受体结合而拮抗白细胞-内皮细胞黏附介导的炎症反应,从而发挥其脑缺血再灌注损伤的保护作用。Objective： To investigate the anti-inflammatory effect of AT1 receptor antagonist,losartan on focal brain ischemia injury in rats and to explore its mechanism. Methods： After 24 hours of reperfusion following 1 hour of cerebral ischemia, the infiltration of neutrophils was investigated by histologireperfusion following 1 hour of cerebral ischemia, the infiltration of neutrophils was investigated by histological examination, the myeloperoxidase （MPO） activity was inspected, and the expression of intercellular adhesion molecule-1 （ICAM-1） was observed by immunohistochemical technique respectively. Results： Losartan could obviously inhibit the number of leukocyte in ischemic brain tissue, the MPO activity and the ICAM-1 expression. Conclusion： Losartan can protect ischemia-reperfusion damage through preventing leukocyte-endothelial cell adhesion, which may be related with its blocking conjugation between Ang Ⅱ and AT1 receptor.

关 键 词：血管紧张素Ⅱ 缺氧缺血 脑 细胞黏附分子 白细胞 过氧化物酶 氯沙坦 

分 类 号：Q95-33[生物学—动物学] R543.3[医药卫生—心血管疾病]