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The role of PI3K/Akt signal pathway in the protective effects of propofol on intestinal and lung injury induced by intestinal ischemia/reperfusion 1

机译:PI3K / Akt信号通路在异丙酚对肠缺血/再灌注所致肠肺损伤的保护作用中的作用1

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Purpose: To investigate the role of PI3k/Akt signal pathway in the protective effects of propofol on intestinal and lung injury induced by intestinal ischemia/reperfusion(I/R). Methods: Male Sprague-Dawley rats were subjected to 45 min of ischemia by occluding the superior mesenteric artery and to 2h of reperfusion to establish the model of I/R. Twenty four rats were randomly divided into four groups: Sham, intestinal I/R (II/R), propofol (P), wortmannin (W). In groups P, W, propofol was injected intravenously and continuously at the onset of reperfusion via infusion pump. PI3K inhibitor (wortmannin) was administered intravenously in group W 25 min before ischemia. Intestinal tissues and lung tissues were obtained for determination of histologic injury, wet/dry weight ratio, malondialdehyde (MDA) levels, superoxide dismutase (SOD) and myeloperoxidase (MPO) activities. Meanwhile, the expressions of caspase-3 and phosphorylated Akt (p-Akt) in intestines and lungs were detected by western blot. Results: Propofol treatment alleviated intestinal and lung morphological changes which were observed in II/R group, Moreover, wet/dry weight ratio, the MDA level, MPO activity and expression of caspase-3 were significantly decreased whereas the SOD activity and p-Akt expression were significantly increased. Notably, the protections were significantly reversed by pretreatment of wortmannin. Conclusion: PI3K/Akt pathway activation play a critical role in the protective effects of propofol on intestinal and lung injury induced by ischemia/reperfusion.
机译:目的:探讨PI3k / Akt信号通路在异丙酚对肠缺血/再灌注(I / R)引起的肠肺损伤的保护作用中的作用。方法:雄性Sprague-Dawley大鼠通过阻塞肠系膜上动脉缺血45分钟,再灌注2h,建立I / R模型。将二十四只大鼠随机分为四组:假手术,肠I / R(II / R),丙泊酚(P),渥曼青霉素(W)。在P,W组中,在重新灌注开始时通过输液泵静脉内和连续注射异丙酚。在缺血前25分钟,在W组中静脉内注射PI3K抑制剂(渥曼青霉素)。获得肠组织和肺组织用于确定组织学损伤,干/湿重比,丙二醛(MDA)水平,超氧化物歧化酶(SOD)和髓过氧化物酶(MPO)活性。同时,通过western blot检测肠和肺中caspase-3和磷酸化Akt(p-Akt)的表达。结果:丙泊酚治疗减轻了II / R组的肠道和肺部形态变化,此外,干/湿重比,MDA水平,MPO活性和caspase-3表达明显降低,而SOD活性和p-Akt降低表达明显增加。值得注意的是,通过渥曼青霉素的预处理可以显着逆转保护作用。结论:PI3K / Akt通路的激活在异丙酚对缺血/再灌注所致肠道和肺损伤的保护作用中起着关键作用。

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