缺血预处理对鼠肺缺血再灌注损伤的保护作用及其机制

Protective mechanism of ischemic preconditioning on the lung ischemia-repurfusion injury in rats

目的探讨缺血预处理(IP)对肺脏缺血再灌注损伤(IRI)的保护机制。方法30只SD大鼠,随机分为预处理组(Ⅰ组)、对照组(C组)和假手术组(S组),每组10只。Ⅰ组和C组大鼠常规开胸后建立左上肺缺血再灌注模型,均遭受了IRI,但Ⅰ组在缺血再灌注前给予IP干预,对以上样本的总蛋白质进行二维凝胶电泳分离,差异表达的蛋白质点进行基质辅助激光解吸电离飞行时间质谱分析鉴定。S组大鼠开胸后不予特殊处理。免疫印迹法比较三组样本中热休克蛋白27 (HSP27)的表达差异。结果建立了分辨率较高、重复性较好的鼠肺IRI双向凝胶电泳参考图谱,45个蛋白质点表达存在差异,其中30个得到了鉴定,HSP27在IP的第一窗口期表达上调。结论HSP27在IP对肺脏IRI的保护机制中起重要作用。

Objective To explore the protective mechanism of isehemic preconditioning （IP） on the lung ischemia-repeffusion injury （IRI）. Methods Thirty SD rats were randomly divided into preconditioning group （group I） ,control group （group C） and sham operation group （group S） （10 animals in each group）. Rat lungs in group I received IP and the following ischemia-reperfusion insults, while those in group C suffered ischemia-reperfusion insults only. The total proteins of those lung samples were separated by means of immobilized pH gradient-based two-dimensional gel eleetrophoresis （2-DE）. The differently expressed spots were identified by matrix-assisted laser desorption/ionization time of flight mass spectrometry and database searching. Rats in group S were not administered with any other intervention after chest incision and lobe dissection. Western blot was employed to compare the HSP27 expression in lung tissues among the groups. Results The study has established the well-resolved, reproducible 2-DE reference map of ischemia-reperfusion injury in rat lung tissue. Forty-five protein spots were differentially expressed and their PMF data showed that 30 proteins could be matched to known protein sequences and unambiguously identified. Western Blot showed that heat shock protein 27 was up-regulated during the classic preconditioning. Conclusion The HSP27 plays a vital role in the protective procession of ischemic preconditioning on lung IRI.