SIN-1抑制缺血再灌注肾脏ICAM-1表达

Inhibitory effect of SIN-1 on ICAM-1 expression in rat kidney after ischemia/reperfusion injury

目的 进一步探讨一氧化氮 (NO)供体SIN 1对急性缺血性肾衰 (IARF)的治疗作用机制。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NO供体对大鼠肾脏缺血再灌注损伤后ICAM 1表达及炎细胞浸润的影响 ,同时进行肾功能测定。结果 肾脏缺血再灌注损伤后ICAM 1表达进行性增强 ,于再灌注 2 4h达峰值 ,以外髓直小血管表达显著 ,整合素 β2阳性细胞同样于再灌注 2 4h达峰值 ,以外髓明显 ;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SIM 1可通过抑制肾组织ICAM 1的表达及炎细胞浸润 。

Objective To explore the therapeutic mechanisms of nitric oxide donor (SIN 1) in ischemic acute renal failure (IARF). Methods The effects of SIN 1 on intercellular adhesion molecule 1 (ICAM 1) expression and inflammatory cell infiltration in rat kidney after ischemia/reperfusion (I/R) injury were examined using ICAM 1, β2 integrin polyclonal antibody, and immunohistochemistry. The renal functions were measured simultaneously. Results Progressive increased expression of ICAM 1 was found in kidneys, especially in vasa recta, after IR injury. β2 integrin positive cells increased simultaneously in the outer medulla. The two indexes reached the peak values at 24 h after I/R injury. SIN 1 infusion at the beginning of reperfusion could remarkably inhibit the enhanced ICAM 1 expression, reduce the local infiltration of inflammatory cells, and ameliorate the renal functions. Conclusion NO donor can inhibit the renal expression of ICAM 1 and the infiltration of leukocytes after ischemia reperfusion injury, which may play an important role in the treatment of ischemic acute renal failure.