摘要
目的 观察缺血再灌注后加用NO供体对肾脏ICAM-1表达及白细胞浸润的影响。方法 分别采用ICAM-1和整合素β2多克隆抗体,免疫组化方法观察加用NO供体后大鼠肾脏缺血再灌注24h ICAM-1表达的变化及肾功能改变。结果 缺血再灌注24h大鼠肾脏ICAM-1及β2阳性细胞表达显著增强,以外髓直小血管,皮质肾小管外毛细血管较为明显。再灌注同时灌注NO供体SIN-1可显著抑制缺血再灌注后ICAM-1的表达增强,减少局部炎细胞浸润,改善肾功能。结论 NO供体可减少肾组织ICAM-1的表达及炎细胞浸润,发挥对急性缺血性肾衰的治疗作用。
Objective To evaluate the effects of nitric oxide donor SIN-1 on the expression of ICAM-1 and leukocytes infiltration in kidneys after ischemic-reperfusion injury. Methods With the use of immunohistochemistry, the changes of the expression of ICAM-1 and β2 integrins were evaluated 24 hours after reperfusion injury with useing of NO donor or not, and the renal function was measured simultaneously. Results Expression of ICAM-1 and p2 positive cells were increased in kidneys 24 hours after reperfusion, especially at vasa recta, peritubular capillaries. SIN-1 infusion at the beginning of reperfusion markedly reduced the staining of ICAM-1 and β2 integrins, and the renal function ameliorated. Conclusion NO donor can reduce the expression of ICAM-1 after renal ischemia-reperfusion injury and reduce the infiltration of leukocytes, The above results suggest that No donor may play a role in the treatment of ischemic acute renal failure.
