一氧化氮合酶在缺血预处理对大鼠肾脏缺血-再灌注损伤保护中的作用

The role of nitric oxide synthase in renal ischemia-reperfusion injury in rats after ischemic preconditioning

目的 :探讨一氧化氮合酶 (NOS)在缺血预处理对大鼠肾脏缺血再灌注损伤保护中的作用。方法 :将大鼠随机分为对照组 (CON)、缺血再灌注组 (IR)和缺血预处理后缺血再灌注组 (IPC)。光镜下观察并行肾小管评分 ,用免疫组化法检测各组中不同灌注时间的 3种 NOS的变化。结果 :不同缺血再灌注时间点病理组织学肾小管评分 IPC组均低于 IR组 (P均 <0 .0 5 ) ,而 IPC组和 CON组之间无显著性差异 (P均 >0 .0 5 ) ;诱导型NOS(i NOS)在 IR组中的表达明显高于 IPC组和 CON组 (P<0 .0 1或 P<0 .0 5 ) ;而内皮型 NOS(e NOS)和神经元型 NOS(n NOS)在各组中的表达无显著性差异 (P均 >0 .0 5 )。结论 :缺血预处理对大鼠肾脏缺血再灌注损伤有保护作用 ,其保护机制与 i NOS的生成减少有关 ;e NOS和 i NOS在缺血预处理过程中无明显变化。

Objective:To investigate the role of nitric oxide synthase (NOS) in renal ischemiareperfusion injury after ischemic preconditioning.Methods:Rats were randomly divided into control group (CON),ischemiareperfusion group (IR),and ischemic preconditioning group (IPC).In various groups,pathological changes were observed and the protein expression of NOS was determined by immunohistochemistry.Results:Scores of renal tubules in IPC were lower than that in IR (all P <0 05),but similar to CON (all P <0 05).The expression of inducible NOS (iNOS) in IR was higher than that in IPC or CON respectively ( P <0 01 or P <0 05),while the expression of endothelial NOS (eNOS) and neural NOS(nNOS) in different groups was similar (all P >0 05).Conclusions:Ischemic preconditioning could protect the damage of ischemiareperfusion to the kidney,and the mechanism may be related to less formation of iNOS.There were no changes in eNOS and nNOS during the process of ischemic preconditioning.