摘要
目的观察缺血预处理对兔肺缺血再灌注性损伤的蛋白质变化,探讨其可能的肺保护机制。方法12只家兔,随机分为预处理组和对照组,每组6只。对照组经历单纯的缺血再灌注损伤,预处理组在缺血再灌注前予以缺血预处理。以二维电泳分离肺组织中的全部蛋白质,应用PDQuest软件寻找差异表达的蛋白质点并以MALDI-TOF质谱仪和Mascot软件对其鉴定。结果研究发现了35个明显差异表达的蛋白质,包括磷酸肌醇3激酶Δ催化亚单位在内的17个蛋白质达到了鉴定。结论通过磷酸肌醇3激酶信号传导通路抑制炎性反应可能是缺血预处理的保护机制。
Objective To investigate the change of the protein expression in lung tissue of rabbits after ischemic preconditioning （IP） and try to elucidate the potential protective mechanism of IP. Methods Twelve domestic rabbits were randomly divided into IP group and control group equally. All the left lungs received ischemiareperfusion injury except that those in group IP were subjected to IP prior to ischemic phase. 2-DE was employed to separate the total protein of the lung tissue. PDQuest analysis software was used to distinguish the differently expressed protein spot. MALDI-TOF-MS and Mascot database searching were exploited to identify these proteins. Results IP attenuated the ischemia-reperfusion lung injury. The proteomic analysis showed 35 target proteins, of which 17 were characterized such as posphatidylinositol 3-kinase （PI3k） delta catalytic subunit. Conclusion That IP inhibits inflammatory cascades through phosphatidylinositol 3-kinase signal transduction pathway may be one of its protective mechanism.
出处
《中华实验外科杂志》
CAS
CSCD
北大核心
2005年第11期1376-1377,共2页
Chinese Journal of Experimental Surgery
基金
中国博士后科学基金资助项目(2004036433)
湖南省卫生厅科研基金资助项目(B2004024)
