摘要
目的研究缺血后处理对鼠肺再灌注损伤肺血管内皮的影响及其可能的保护作用机制。方法雄性SD大鼠24只，随机分为假手术对照组（Sham组）、缺血－再灌注组（I—R组）和缺血后处理组（IPostC组），每组8只。三组实验结束后均留取左肺组织及动脉血，血液用于测定内皮素－1（ET－1）水平（ELISA法），肺组织制作成10％组织匀浆，用于测定髓过氧化物酶（MPO）、丙二醛（MDA）及超氧化物歧化酶（SOD）水平，RT—PCR法检测肺组织中ACEmRNA的表达。留取小块肺组织测定肺湿／干质量比（W／D），并在光镜下观察肺组织的病理形态。结果三组间各项指标比较差异均有统计学意义（P〈0．05）。与Sham组比较，I—R组MPO、MDA、W／D和ET－1水平及肺组织中ACEmRNA的表达量均明显升高（P〈0．05），而SOD水平明显降低（P〈0．05），光镜下观察见I—R组肺组织炎症反应明显加重；与I—R组比较，IPostC组MPO、MDA、W／D和ET－1水平及肺组织中ACEmRNA的表达量均明显降低（P〈0．05），而SOD水平明显升高（P〈0．05），光镜下观察见IPostC组肺组织炎症反应明显减轻。结论缺血后处理能够减轻鼠肺缺血－再灌注损伤，其机制可能与抑制缺血－再灌注肺血管内皮细胞释放ET－1、下调肺血管内皮ACEmRNA的表达、减少肺组织中氧自由基的产生和中性粒细胞在肺内的聚集及保护抗氧化系统有关。
Objective To investigate the protective effect of ischemic postconditioning on puhnonary vascular endothelium during ischemia reperfusion injury in rats and to analyze its possible mechanisms. Methods 24 male rats were randomly divided into three groups ： sham group （ n = 8 ）, ischemia reperfusion group （I- R group, n = 8 ） , ischemic postconditioning group （IPostC group, n = 8）. The left lung tissues and arterial blood were preserved at the end of three group experiments. The blood was prepared to detect the level of endothelin - 1 by ELISA. The parts of left lung tissue were made into homogenate, that was prepared to detect the concentration of MPO, MDA and SOD. Meanwhile, ACE mRNA expression of lung tissue was measured by RT - PCR. The wet to dry weight ratio （W/D） was measured at the end of experiment, and the lung tissue was prepared for light microscopic morphological observation. Results There was significant difference among the 3 groups （P 〈 0.05）. The expression of ACE mRNA, the levels of MPO, MDA, ET - 1 and W/D in the lung significantly increased in I - R group compared to sham group （ P 〈 0.05 ） , but the levels of SOD was significantly lower（P 〈 0.05 ）. The lung histological examination showed that the inflammation in the lung of I - R group was significantly serious than that in the control group. The expression of ACE mRNA,the levels of MPO, MDA, ET - 1 and W/D in the lung in the IPostC group were significantly decreased compared to I -R group（P 〈0.05 ）, and the levels of SOD was significantly increased（ P 〈 0. 05 ）. The lung histological examination showed that the inflammation in the lung of IPostC group was significantly decreased compared to I - R group. Conclusion Ischemic postconditioning can reduce significantly ischemia - reperfusion injury of lung in rats. The possible mechanism is that postconditioning may inhibit pulmonary endothelial ET - 1 release, reduce the expression of ACE mRNA in pulmonary vascular endothelium, decrease the level of
出处
《中国急救医学》
CAS
CSCD
北大核心
2011年第7期610-614,F0003,共6页
Chinese Journal of Critical Care Medicine
基金
基金项目：贵州省科学技术基金资助项目（黔科合J字[2009]2313号）
关键词
缺血后处理
再灌注损伤
肺
血管内皮
血管紧张素转换酶
Ischemic postconditioning
Ischemia - reperfusion injury
Lung
Vascular endothelium
Angiotensin -converting enzyme
