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出 处:《临床麻醉学杂志》2014年第6期606-609,共4页Journal of Clinical Anesthesiology
基 金:国家自然科学基金资助项目(30571785;30972862);四川省科技支撑计划项目(2012FZ0121)
摘 要:目的探讨缺血-再灌注(IR)对肺钠氢交换蛋白-1(NHE-1)表达的影响,及卡立泊来德(cariporide)预处理能否通过抑制NHE-1表达减轻肺组织的炎症损伤。方法 20枚离体灌注的大鼠肺随机分为四组:对照组(C组)、IR组、NHE-1激活剂LiCl预处理组(LiCl组)和cariporide预处理+缺血-再灌注组(CIR组)。再灌注结束后,免疫组化检测肺组织中NHE-1蛋白表达,HE染色观察肺组织病理学改变并行病理评分。结果与C组和CIR组比较,IR组和LiCl组NHE-1表达明显增加(P<0.05),CIR组和C组差异无统计学意义。IR组和LiCl组肺组织病理切片均观察到明显炎症损伤,病理评分明显高于C组和CIR组(P<0.05),CIR组病理评分和C组差异无统计学意义。结论离体的IR大鼠肺组织,NHE-1表达增加,选择性NHE-1抑制剂cariporide能减轻IR导致的肺组织炎症损伤。Objective To investigate the expression of Na+/H+ exchanger isoform-1 (NHE-1) during ischemia-reperfusion (IR) in rat lung tissue and determine whether cariporide preconditioning protects lung from inflammatory injury via inhibiting NHE-1 protein expression. Methods Twenty i- solated perfused lungs were randomly divided into 4 groups: the lungs in control group (group C) were continuously perfused for 120 min; the lungs in group IR were subjected to 30 min perfusion, followed by 60 rain ischemia and 30 min reperfusion; in group LiC1 preconditioning, the lungs were preconditioned with LiCl for 30 min, then continuously perfused for 90 rain; in cariporide preconditioning+IR (CIR) group, the lungs were preconditioned with cariporide for 30 min, following 60 min ischemia and 30 min reperfusion. After reperfusion, the NHE-1 protein expression was determined by immunohistochemistry and the histopathologic change and pathology scores were ascertained from HE sections. Results The NHE-1 protein expression in lung tissue in groups IR and LiCI were significantly increased compared with groups C and CIR (P〈0.05), and there was no difference between groups C and CIR. Histological examination revealed marked inflammatory changes in groups IR and LiCl, whereas no significant changes in lungs of groups C and CIR. The pathology score of lung in groups IR and LiCl were higher than that in groups C and CIR (P〈0. 05), and there was no difference between the last two groups. Conclusion IR results in an increased NHE1 protein expression in rat isolated perfused lung, and the selective NHE-1 inhibitor cariporide could repress the NHE-1 protein expression, thereby decrease the lung inflammatory injury after IR.
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