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Proteomic study on protective mechanism of ischemic preconditioning to ischemia-reperfusion lung injury

机译:蛋白质组学研究缺血预处理对缺血再灌注肺损伤的保护机制

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Objective To investigate the change of protein expression of lung tissue of rabbit after ischemic preconditioning (IP) and try to elucidate the potential protective mechanism of IP. Methods 12 domestic rabbits were randomly divided into group IP and group control(6 rabbits in each group). All the left lungs were afflicted by ische mia-reperfusion injury except that those in group IP were subject 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 1) IP attenuated the ischemia-reperfusion lung injury. 2) The proteomic analysis showed 35 target proteins, of which 17 were characterized such as phosphatidylinositol 3-kinase(PI3k) delta catalytic subunit. Conclusions 1) Proteomic is a promising tool to investigate the IP and ischemia-reperfusion lung injury. 2) That IP inhibits inflammatory cascades through phosphatidylinositol 3-kinase signal transduction pathway may be one of its protective mechanism.
机译:目的探讨缺血预处理(IP)后家兔肺组织蛋白质表达的变化,并试图阐明其可能的保护机制。方法12只家兔随机分为IP组和对照组(每组6只)。 IP组中的所有左肺均受到缺血再灌注损伤的伤害,但IP组中的那些在缺血阶段之前接受了IP。使用2-DE分离肺组织的总蛋白。 PDQuest分析软件用于区分不同表达的蛋白斑点。利用MALDI-TOF-MS和Mascot数据库搜索来鉴定这些蛋白质。结果1)IP减轻了缺血再灌注肺损伤。 2)蛋白质组学分析显示35种靶蛋白,其中17种具有特征性,如磷脂酰肌醇3-激酶(PI3k)δ催化亚基。结论1)蛋白质组学是研究IP和缺血再灌注肺损伤的有前途的工具。 2)IP通过磷脂酰肌醇3激酶信号转导通路抑制炎症级联反应可能是其保护机制之一。

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