Role of adiponectin in diabetes myocardial ischemia-reperfusion injury and ischemic postconditioning

Abstract Purpose Patients with diabetes are vulnerable to myocardial I/R (ischaemia/reperfusion) injury, but are not responsive to IPO (ischaemic post-conditioning). We hypothesized that decreased cardiac Adiponectin (APN) is responsible for the loss of diabetic heart sensitivity to IPO cardioprotecton. Methods Diabetic rats were subjected to I/R injury (30 min of LAD occlusion followed by 120 min of reperfusion). Myocardial infarct area was determined by TTC staining. Cardiac function was monitored by a microcatheter. ANP, 15-F2t-isoprostane, nitrotyrosine and MDA were measured by assay kits. Levels of p-Akt, total-Akt and GAPDH were determined by Western Blot. Results Diabetic rats subjected to myocardial IR exhibited severe myocardial infarction and oxidative stress injury, lower APN in the plasma and cardiac p-Akt expression ( P <0.05). IPO significantly attenuated myocardial injury and up-regulated plasma APN content and cardiac p-Akt expression in non-diabetic rats but not in diabetic rats. Linear correlation analysis showed that the expression of adiponectin was positively correlated with p-Akt and negatively correlated with myocardial infarction area ( P <0.01). Conclusion Protective effect of IPO was tightly correlated with the expression of adiponectin, exacerbation of I/R injury and ineffectiveness of IPO was partially due to the decline of adiponectin and inactivation of Akt in diabetes mellitus.

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Main Authors: Cao,Chen, Liu,Hui-min, Li,Wei, Wu,Yang, Leng,Yan, Xue,Rui, Chen,Rong, Tang,Ling-hua, Sun,Qian, Xia,Zhongyuan, Tang,Qi-zhu, Shen,Di-fei, Meng,Qing-tao
Format: Digital revista
Language:English
Published: Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia 2020
Online Access:http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0102-86502020000100204
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spelling oai:scielo:S0102-865020200001002042020-03-18Role of adiponectin in diabetes myocardial ischemia-reperfusion injury and ischemic postconditioningCao,ChenLiu,Hui-minLi,WeiWu,YangLeng,YanXue,RuiChen,RongTang,Ling-huaSun,QianXia,ZhongyuanTang,Qi-zhuShen,Di-feiMeng,Qing-tao Adiponectin Diabetes Reperfusion Injury Ischemic Postconditioning Abstract Purpose Patients with diabetes are vulnerable to myocardial I/R (ischaemia/reperfusion) injury, but are not responsive to IPO (ischaemic post-conditioning). We hypothesized that decreased cardiac Adiponectin (APN) is responsible for the loss of diabetic heart sensitivity to IPO cardioprotecton. Methods Diabetic rats were subjected to I/R injury (30 min of LAD occlusion followed by 120 min of reperfusion). Myocardial infarct area was determined by TTC staining. Cardiac function was monitored by a microcatheter. ANP, 15-F2t-isoprostane, nitrotyrosine and MDA were measured by assay kits. Levels of p-Akt, total-Akt and GAPDH were determined by Western Blot. Results Diabetic rats subjected to myocardial IR exhibited severe myocardial infarction and oxidative stress injury, lower APN in the plasma and cardiac p-Akt expression ( P <0.05). IPO significantly attenuated myocardial injury and up-regulated plasma APN content and cardiac p-Akt expression in non-diabetic rats but not in diabetic rats. Linear correlation analysis showed that the expression of adiponectin was positively correlated with p-Akt and negatively correlated with myocardial infarction area ( P <0.01). Conclusion Protective effect of IPO was tightly correlated with the expression of adiponectin, exacerbation of I/R injury and ineffectiveness of IPO was partially due to the decline of adiponectin and inactivation of Akt in diabetes mellitus.info:eu-repo/semantics/openAccessSociedade Brasileira para o Desenvolvimento da Pesquisa em CirurgiaActa Cirúrgica Brasileira v.35 n.1 20202020-01-01info:eu-repo/semantics/articletext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0102-86502020000100204en10.1590/s0102-865020200010000007
institution SCIELO
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country Brasil
countrycode BR
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databasecode rev-scielo-br
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libraryname SciELO
language English
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author Cao,Chen
Liu,Hui-min
Li,Wei
Wu,Yang
Leng,Yan
Xue,Rui
Chen,Rong
Tang,Ling-hua
Sun,Qian
Xia,Zhongyuan
Tang,Qi-zhu
Shen,Di-fei
Meng,Qing-tao
spellingShingle Cao,Chen
Liu,Hui-min
Li,Wei
Wu,Yang
Leng,Yan
Xue,Rui
Chen,Rong
Tang,Ling-hua
Sun,Qian
Xia,Zhongyuan
Tang,Qi-zhu
Shen,Di-fei
Meng,Qing-tao
Role of adiponectin in diabetes myocardial ischemia-reperfusion injury and ischemic postconditioning
author_facet Cao,Chen
Liu,Hui-min
Li,Wei
Wu,Yang
Leng,Yan
Xue,Rui
Chen,Rong
Tang,Ling-hua
Sun,Qian
Xia,Zhongyuan
Tang,Qi-zhu
Shen,Di-fei
Meng,Qing-tao
author_sort Cao,Chen
title Role of adiponectin in diabetes myocardial ischemia-reperfusion injury and ischemic postconditioning
title_short Role of adiponectin in diabetes myocardial ischemia-reperfusion injury and ischemic postconditioning
title_full Role of adiponectin in diabetes myocardial ischemia-reperfusion injury and ischemic postconditioning
title_fullStr Role of adiponectin in diabetes myocardial ischemia-reperfusion injury and ischemic postconditioning
title_full_unstemmed Role of adiponectin in diabetes myocardial ischemia-reperfusion injury and ischemic postconditioning
title_sort role of adiponectin in diabetes myocardial ischemia-reperfusion injury and ischemic postconditioning
description Abstract Purpose Patients with diabetes are vulnerable to myocardial I/R (ischaemia/reperfusion) injury, but are not responsive to IPO (ischaemic post-conditioning). We hypothesized that decreased cardiac Adiponectin (APN) is responsible for the loss of diabetic heart sensitivity to IPO cardioprotecton. Methods Diabetic rats were subjected to I/R injury (30 min of LAD occlusion followed by 120 min of reperfusion). Myocardial infarct area was determined by TTC staining. Cardiac function was monitored by a microcatheter. ANP, 15-F2t-isoprostane, nitrotyrosine and MDA were measured by assay kits. Levels of p-Akt, total-Akt and GAPDH were determined by Western Blot. Results Diabetic rats subjected to myocardial IR exhibited severe myocardial infarction and oxidative stress injury, lower APN in the plasma and cardiac p-Akt expression ( P <0.05). IPO significantly attenuated myocardial injury and up-regulated plasma APN content and cardiac p-Akt expression in non-diabetic rats but not in diabetic rats. Linear correlation analysis showed that the expression of adiponectin was positively correlated with p-Akt and negatively correlated with myocardial infarction area ( P <0.01). Conclusion Protective effect of IPO was tightly correlated with the expression of adiponectin, exacerbation of I/R injury and ineffectiveness of IPO was partially due to the decline of adiponectin and inactivation of Akt in diabetes mellitus.
publisher Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia
publishDate 2020
url http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0102-86502020000100204
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