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肺缺血再灌注损伤时血浆中介素及其肺脏受体系统的变化 被引量:1

Changes of plasma intermedin and its receptor system in lung ischemia-reperfusion injury
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摘要 目的观察大鼠肺缺血再灌注损伤中介素(IMD)及其受体的变化情况及其意义。方法建立大鼠在体肺缺血冉灌注模型。将健康雄性Wistar大鼠72只随机分为手术对照组(C组)、缺血再灌注组(IR组)、IMD153药物干预组(D组)。每组分别存缺血45min和再灌注60、120min3个时点处死8只大鼠,取血浆和行肺中叶,放射免疫法测定血浆IMD含量,RTPCR测定肺组织IMD、降钙素受体样受体(CL)、受体活性修饰蛋白(RAMP)1、2、3mRNA表达水平;并进行肺组织病理学检查。结果与C组相比,再灌注期间IR组肺组织中IMD、CL和RAMP1、2、3mRNA表达水平及血浆中IMD含量降低(P值均〈0.05),而经IMD153干预后可以减弱缺血再灌注诱导上述指标的变化,肺组织病理学检查显示肺缺血再灌注损伤程度也较IR组明显减轻。结论IMD及其受体系统参与了肺缺血再灌注损伤的发病过程,可能起保护作用。 Objective To investigate the changes of internledin (IMI)) and its receptor system in lung ischemia reperfusion injury rats and its significance. Methods The rat model of lung ischemia reperfusion was made. Seventy two healthy male Wistar rats were randomly divided into three groups: surgical control group (C group),ischemia-reperfusion group (IR group) and IMD1 53 pretrcated group (1) group). At 45 min after ischemia,60 rain and 120 rain after reperfusion,eight rats in each group were sacrificed,plasma and middle lobe of right lung were collected. The plasma IMD content was determined by radioirnmunoassay,the mRNA levels of IMD,calcitonin receptor-like receptor (CL),receptor activitymodifying protein (RAMP)1,2,3 in lung were determined by RT-P(TR,and the histopathological study of lung tissue was also performed. Resalts The plasma IMD content of and the mRNA expression of IMD, CL,RAMP1,2,3 in lung tissue in IR group were lower than those in C group during reperfusion (all P 0.05). After pretreamented by IMD1 53,the changes of these indicators induced by ischemia reperfusion were relieved,histopathological examination showed that the degree of lung ischemia reperfusion injury also significantly improved. Conclusions IMD and its receptor system are involved in the pathogencsis of lung ischemia reperfusion injury,and may play a protective role.
出处 《国际呼吸杂志》 2011年第6期431-435,共5页 International Journal of Respiration
基金 山西省留学人员管理委员会办公室科研资助项目(200810)
关键词 肺缺血再灌注损伤 中介素 降钙素受体样受体 受体活性修饰蛋白 保护 Lung ischemia-reperfusion injury Intcrmedin Calcitonin receptor like receptor Receptor activity-modifying protein Protection
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