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作 者:周留正[1] 孙浩[1] 贾俊海[2] 潘伟[2] 马尘超[3] 何悦成[3] 姜蓉瑛[3]
机构地区:[1]江苏大学附属医院泌尿外科,江苏镇江2120001 [2]江苏大学基础医学与医学技术学院,江苏镇江212013 [3]江苏大学临床医学院,江苏镇江212013
出 处:《江苏大学学报(医学版)》2009年第2期125-127,131,I0002,共5页Journal of Jiangsu University:Medicine Edition
基 金:镇江市科技发展基金资助项目(SH2008032)
摘 要:目的:观察缺血预处理后大鼠缺血再灌注肾脏氧化亚氮、氧化亚氮合酶水平和L-选择素表达的变化,探讨肾缺血预处理对肾缺血再灌注损伤的影响。方法:SD大鼠30只,分为假手术组、缺血再灌注组、缺血预处理组,于手术后2小时取血、肾组织检测氧化亚氮(NO)含量、氧化亚氮合酶(NOS)活性、超氧化物歧化酶(SOD)活性、丙二醛(MDA)活性,免疫组化法检测肾组织L-选择素(L-selectin)的表达水平。结果:缺血预处理组SOD活性明显高于缺血再灌注组(P<0.01),缺血预处理组MDA含量明显低于缺血再灌注组(P<0.01),缺血预处理组NOS,NO水平明显高于缺血再灌注组(P<0.01),缺血预处理组L-选择素表达明显低于缺血再灌注组(P<0.05)。结论:缺血预处理减轻肾缺血再灌注损伤的机制可能是增加NOS在血、肾脏的表达,抑制L-选择素的表达,进而维持肾SOD活力,减少MDA含量。Objective: To observe the change of NO, NOS and L-selectin expression in rat renal ischemic reperfusion injury after renal ischemic preconditioning and investigate the effect of ischemic preconditioning on renal ischemic reperfusion injury. Methods: Thirty SD rats were randomly divided into three groups: sham-operated group, ischemic-reperfusion group, ischemic preconditioning group. The renal underwent 60-minute ischemic and 2-hour reperfusion. The level of Superoxide Dismutase ( SOD), Malondial-dehyde ( MDA), NO, NOS of kidney, blood in each group were examined, L-selectin expression in kidney was tested with immunohistochemichemistry. Results: SOD: The values in ischemic-preconditioning group were significantly higher than that in ischemic-reperfusion group ( P 〈 0.01 ), MDA : The values in ischemic-preconditioning group were significantly lower than that in ischemic-reperfusion group ( P 〈 0.01 ), NOS, NO:The values in ischemic-preconditioning group were significantly higher than that in ischemic- reperfusion group. The expression of L-selectin in ischemic-preconditioning group was lower than that in ischemic-reperfusion group(P 〈 0.05 ). Conclusion: Ischemic preconditioning could protect kidney from ischemic reperfusion injury, the mechanism might be that it increased NOS in kidneys and blood, so that the expression of L-selection was inhibited, with improving the SOD's activity and reducing the levels of MDA in kidney and blood.
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