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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。
Objective: To investigate the role and significance of heat shock protein 27 (HSP27) in the protection of lung ischemic preconditioning. Methods: Thirty rabbits were randomly divided into three groups: sham (S) group, ischemia / reperfusion (I / R) group and ischemia Pretreatment (PC) group, the ratio of wet to dry weight ratio and the number of alveolar damage in lung tissue was detected by experiment, ultrastructural damage of lung tissue was evaluated by electron microscope, and the localization and expression of heat shock protein 27 in lung tissue were detected by immunohistochemistry. Results: (1) The ratio of W / D and IAR in I / R group was significantly higher than that in S group (all P <0.01); W / D and IAR in PC group were significantly lower than those in I / R Group (P <0.05 or P <0.01). ② Immunohistochemistry showed strong expression of HSP27 in the intima and adventitial layer of pulmonary arterioles, pulmonary venous wall in all groups, distal respiratory bronchioles and some alveolar epithelial cells in PC group. HSP27 content (average absorbance value LD) Higher than I / R group and S group (all P <0.01). ③I / R group lung tissue ultrastructural damage was significantly, while the PC group was significantly reduced injury. Conclusion: Pulmonary ischemia preconditioning can reduce lung ischemia-reperfusion injury, HSP27 expression and participate in the protection of pulmonary ischemic preconditioning.