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PI3K在机械通气肺损伤中的作用及对细胞因子影响

he Mechanisms of PI3K to Prevent Lung Injury Induced by Mechanical Ventilation

中文摘要英文摘要

目的 观察过度机械通气大鼠不同组织中的TNF-a和MIP-2变化以及磷脂酰肌醇3激酶(PI3K)抑制剂(LY294002)对其影响。方法 将 48只大鼠随即分为空白组(A)、正常通气组(B)、过度通气组(C)、过度通气+LPS组(D)、过度通气+LY294002组(E)、过度通气+LPS+LY294002组(F)。过度机械通气4h后,采用双抗体夹心ELISA方法测定各组肺匀浆、血浆、肺泡灌洗液中(BALF)的TNF-a和MIP-2含量。结果 C和D组三种组织中的TNF-a和MIP-2均较A和B组显著升高(p<0.05);而在同一组中,肺组织和BALF中的二者含量增加较血浆显著;使用LY294002后肺匀浆和BALF中的TNF-a和MIP-2可显著降低(E、F组与C和D组比较,p<0.001)。结论 过度机械通气和/或合并LPS可导致肺组织炎症性损害,PI3K抑制剂LY294002可显著抑制TNF-a和MIP-2的生成,该炎症性损害可能部分是由于PI3K参与所致。

bjective To observe the effects of phosoinositide 3-OH kinase inhibition on ventilation-induced lung injury by detecting the levels of TNF-a and MIP-2. Methods 48 Sprague-Dawley rats were randomized into six groups (n=8): Group A: non-ventilation ;Group B: low-volume ventilation(LVT) : VT 6 ml/kg with zero PEEP and room air inspiration , RR40breaths/min ; Group C:high-volume(HVT) : VT 45ml/ kg with zero PEEP , RR40breaths/min ; Group D:LPS+HVT ;Group E: ly294002+HVT ; Group F: ly294002+ LPS+HVT . After 4 h of ventilation , Cytokine concentrations of TNF-a and macrophage inflammatory protein-2 [MIP-2]) were measured by ELISA. Results TNF-a and MIP-2 concentrations in groups C and D in the lung homogenate and BALF were increased significantly compared with the groups of A and B , However when ly294002 were injected via vein , TNF-a and MIP-2 were decreased notably in groups E and F .Otherwise they were much higher than that of serum concentrations at the same groups (p<0.05).

王月兰、姚尚龙、武庆平

基础医学

机械通气肺损伤, 细胞炎症因子 ,磷脂酰肌醇脂激酶

ventilation-induced lung injuryytokinePhosphoinositide 3-kinase

王月兰,姚尚龙,武庆平.PI3K在机械通气肺损伤中的作用及对细胞因子影响[EB/OL].(2005-01-26)[2025-05-25].http://www.paper.edu.cn/releasepaper/content/200501-95.点此复制

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