热休克蛋白27参与兔肺缺血预处理保护

目的：探讨热休克蛋白27（HSP27）在肺缺血预处理保护中所起的作用及意义。方法：采用在体兔单肺原位缺血再灌注模型,30只日本大耳兔随机均分为三组：假手术（S）组、缺血/再灌注（I/R）组及缺血预处理（PC）组,实验检测肺组织湿干重比和肺泡损伤数比值,电镜评定肺组织超微结构损伤,免疫组化检测肺组织热休克蛋白27的定位及表达。结果：①I/R组肺组织湿干重比（W/D）及肺泡损伤数比值（IAR）明显于S组（均P〈0.01）;PC组W/D及IAR均显著低于I/R组（P〈0.05或P〈0.01）。②免疫组化显示PC组肺小动脉内膜及外膜层、肺小静脉壁全层、远端呼吸性细支气管及少许肺泡上皮HSP27有强表达;肺小静脉HSP27含量（平均吸光度值LD）高于I/R组和S组（均P〈0.01）。③I/R组肺组织超微结构的损伤明显,而PC组损伤明显减轻。结论：肺缺血预处理能减轻肺缺血再灌注损伤,HSP27表达增加并参与肺缺血预处理保护。

Heat shock protein-27 participated in the protection of lung ischemic preconditioning in rabbit

Objective： To investigate the effect and significance of heat shock protein-27 in the protection afforded by lung ischemic preconditioning in rabbits. Methods： Single lung in situ ischemic reperfusion animal model was used. 30 rabbits were randomly divided into three groups： sham （S） group, ischemic/reperfusion （I/R） group and ischemic preconditioning （PC） group. Wet to dry ratio （W/D） and injured aiveoli rate （IAR） were determined. Ultramicroscopic structural change was observed under electron microscope. Heat shock protein-27 was detected with immunohistochemistry. Results：①W/D and IAR in I/R group were higher than that in S group （P〈0.01）. The W/D and IAR in PC group were lower than that in I/R group （P〈0.05, P〈0.01 respectively）. ②The heat shock protein-27 strongly expressed in intima and extima of smaii pulmonary artery, vessel wail of small puimonary vein, respiratory brochiole and part of alveolar epitheiium. The light density of heat shock protein-27 in small pulmonary veins in PC group was higher than that of other groups. ③Electron microscope showed serious iung injury occurred in I/ R group while there was no significant injury in PC group. Conclusion： Lung ischemic preconditioning can mitigate lung ischemia reperfusion injury,highly expressed heat shock protein-27 participated in the protection afforded by lung ischemic preconditioning.