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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

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 2...

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Autores principales: Li, Qingwen, Cui, Shanshan, Jing, Guoqing, Ding, Huang, Xia, Zhongyuan, He, Xianghu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6585923/
https://www.ncbi.nlm.nih.gov/pubmed/30785506
http://dx.doi.org/10.1590/s0102-865020190010000005
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author Li, Qingwen
Cui, Shanshan
Jing, Guoqing
Ding, Huang
Xia, Zhongyuan
He, Xianghu
author_facet Li, Qingwen
Cui, Shanshan
Jing, Guoqing
Ding, Huang
Xia, Zhongyuan
He, Xianghu
author_sort Li, Qingwen
collection PubMed
description 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.
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spelling pubmed-65859232019-07-02 The role of PI3K/Akt signal pathway in the protective effects of propofol on intestinal and lung injury induced by intestinal ischemia/reperfusion Li, Qingwen Cui, Shanshan Jing, Guoqing Ding, Huang Xia, Zhongyuan He, Xianghu Acta Cir Bras ORIGINAL ARTICLES 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. Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia 2019-02-14 /pmc/articles/PMC6585923/ /pubmed/30785506 http://dx.doi.org/10.1590/s0102-865020190010000005 Text en https://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License
spellingShingle ORIGINAL ARTICLES
Li, Qingwen
Cui, Shanshan
Jing, Guoqing
Ding, Huang
Xia, Zhongyuan
He, Xianghu
The role of PI3K/Akt signal pathway in the protective effects of propofol on intestinal and lung injury induced by intestinal ischemia/reperfusion
title The role of PI3K/Akt signal pathway in the protective effects of propofol on intestinal and lung injury induced by intestinal ischemia/reperfusion
title_full The role of PI3K/Akt signal pathway in the protective effects of propofol on intestinal and lung injury induced by intestinal ischemia/reperfusion
title_fullStr The role of PI3K/Akt signal pathway in the protective effects of propofol on intestinal and lung injury induced by intestinal ischemia/reperfusion
title_full_unstemmed The role of PI3K/Akt signal pathway in the protective effects of propofol on intestinal and lung injury induced by intestinal ischemia/reperfusion
title_short The role of PI3K/Akt signal pathway in the protective effects of propofol on intestinal and lung injury induced by intestinal ischemia/reperfusion
title_sort role of pi3k/akt signal pathway in the protective effects of propofol on intestinal and lung injury induced by intestinal ischemia/reperfusion
topic ORIGINAL ARTICLES
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6585923/
https://www.ncbi.nlm.nih.gov/pubmed/30785506
http://dx.doi.org/10.1590/s0102-865020190010000005
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