Glucagon Like Peptide-1 is Protective Against Myocardial Ischemia/Reperfusion Injury when Given Either as a Preconditioning Mimetic or at Reperfusion in an Isolated Rat Heart Model

2005 ◽  
Vol 19 (1) ◽  
pp. 9-11 ◽  
Author(s):  
Amal K. Bose ◽  
Mihaela M. Mocanu ◽  
Richard D. Carr ◽  
Derek M. Yellon
Keyword(s):  
Myocardial Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Isolated Rat Heart ◽  
Heart Model ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Myocardial Ischemia Reperfusion ◽  
Isolated Rat

An interaction between glucagon-like peptide-1 and adenosine contributes to cardioprotection of a dipeptidyl peptidase 4 inhibitor from myocardial ischemia-reperfusion injury

2015 ◽  
Vol 308 (10) ◽  
pp. H1287-H1297 ◽  
Author(s):  
Madoka Ihara ◽  
Hiroshi Asanuma ◽  
Satoru Yamazaki ◽  
Hisakazu Kato ◽  
Yoshihiro Asano ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Dipeptidyl Peptidase 4 ◽  
Dpp4 Inhibitor ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Myocardial Ischemia Reperfusion

Dipeptidyl peptidase 4 (DPP4) inhibitors suppress the metabolism of the potent antihyperglycemic hormone glucagon-like peptide-1 (GLP-1). DPP4 was recently shown to provide cardioprotection through a reduction of infarct size, but the mechanism for this remains elusive. Known interactions between DPP4 and adenosine deaminase (ADA) suggest an involvement of adenosine signaling in DPP4 inhibitor-mediated cardioprotection. We tested whether the protective mechanism of the DPP4 inhibitor alogliptin against myocardial ischemia-reperfusion injury involves GLP-1- and/or adenosine-dependent signaling in canine hearts. In anesthetized dogs, the coronary artery was occluded for 90 min followed by reperfusion for 6 h. A 4-day pretreatment with alogliptin reduced the infarct size from 43.1 ± 2.5% to 17.1 ± 5.0% without affecting collateral flow and hemodynamic parameters, indicating a potent antinecrotic effect. Alogliptin also suppressed apoptosis as demonstrated by the following analysis: 1) reduction in the Bax-to-Bcl2 ratio; 2) cytochrome c release, 3) an increase in Bad phosphorylation in the cytosolic fraction; and 4) terminal deoxynucleotidyl transferase dUTP nick end labeling assay. This DPP4 inhibitor did not affect blood ADA activity or adenosine concentrations. In contrast, the nonselective adenosine receptor blocker 8-( p-sulfophenyl)theophylline (8SPT) completely blunted the effect of alogliptin. Alogliptin did not affect Erk1/2 phosphorylation, but it did stimulate phosphorylation of Akt, glycogen synthase kinase-3β, and cAMP response element-binding protein (CREB). Only 8SPT prevented alogliptin-induced CREB phosphorylation. In conclusion, the DPP4 inhibitor alogliptin suppresses ischemia-reperfusion injury via adenosine receptor- and CREB-dependent signaling pathways.

scholarly journals Transient Acidosis during Early Reperfusion Attenuates Myocardium Ischemia Reperfusion Injury via PI3k-Akt-eNOS Signaling Pathway

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Xin Qiao ◽  
Jinjin Xu ◽  
Qing-Jun Yang ◽  
Yun Du ◽  
Shaoqing Lei ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Early Reperfusion ◽  
Rat Hearts ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion ◽  
Myocardium Ischemia Reperfusion ◽  
Isolated Rat

In this paper, we concluded that transient acidosis reperfusion conferred cardioprotection against myocardial ischemia reperfusion injury in isolated rat hearts through activating PI3K-Akt-eNOS pathway.

Endoxin-mediated myocardial ischemia reperfusion injury in rats in vitro

2004 ◽  
Vol 82 (6) ◽  
pp. 402-408 ◽  
Author(s):  
Yong-Sheng Ke ◽  
He-Gui Wang ◽  
De-Guo Wang ◽  
Gen-Bao Zhang
Keyword(s):  
Myocardial Ischemia ◽  
Cardiac Function ◽  
Atpase Activity ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Rat Hearts ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion ◽  
Isolated Rat

Myocardial ischemia reperfusion results in an increase in intracellular sodium concentration, which secondarily increases intracellular calcium via Na+-Ca2+ exchange, resulting in cellular injury. Endoxin is an endogenous medium of digitalis receptor and can remarkably inhibit Na+/K+-ATPase activity. Although the level of plasma endoxin is significantly higher during myocardial ischemia, its practical significance is unclear. This research is to investigate whether endoxin is one of important factors involved in myocardial ischemia reperfusion injury. Ischemia reperfusion injury was induced by 30 min of global ischemia and 30 min of reperfusion in isolated rat hearts. Heart rate (HR), left ventricular developed pressure (LVDP), and its first derivative (±dp/dtmax) were recorded. The endoxin contents, intramitochondrial Ca2+ contents, and the Na+/K+-ATPase activity in myocardial tissues were measured. Myocardial damages were evaluated by electron microscopy. The endoxin and intramitochondrial Ca2+ contents in myocardial tissues were remarkably higher, myocardial membrane ATPase activity was remarkably lower, the cardiac function was significantly deteriorated, and myocardial morphological damages were severe in myocardial ischemia reperfusion group vs. control. Anti-digoxin antiserum (10, 30 mg/kg) caused a significant improvement in cardiac function (LVDP and ±dp/dtmax), Na+/K+-ATPase activity, and myocardial morphology, and caused a reduction of endoxin and intramitochondrial Ca2+ contents in myocardial tissues. In the present study, the endoxin antagonist, anti-digoxin antiserum, protected the myocardium against the damages induced by ischemia reperfusion in isolated rat hearts. The results suggest that endoxin might be one of main factors mediating myocardial ischemia reperfusion injury.Key words: endoxin, anti-digoxin antiserum, myocardial reperfusion injury, morphological evaluation, Na+/K+-exchanging ATPase.

scholarly journals Cardioprotective Effects of Astragalin against Myocardial Ischemia/Reperfusion Injury in Isolated Rat Heart

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Daoxu Qu ◽  
Jichun Han ◽  
Huanhuan Ren ◽  
Wenxiao Yang ◽  
Xinjie Zhang ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Rat Heart ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Isolated Rat Heart ◽  
Sprague Dawley ◽  
Sod Activity ◽  
Cardioprotective Effects ◽  
Myocardial Ischemia Reperfusion ◽  
Isolated Rat

This study aims to evaluate the cardioprotective effects of astragalin against myocardial ischemia/reperfusion (I/R) injury in isolated rat heart. The cardioprotective effects of astragalin on myocardial I/R injury were investigated on Langendorff apparatus. Adult male Sprague-Dawley rats were randomly divided into five groups. The results showed that astragalin pretreatment improved myocardial function. Compared with I/R group, lactate dehydrogenase (LDH) and creatine kinase (CK) activities in coronary flow decreased in astragalin pretreatment groups, whereas superoxide dismutase (SOD) activity and glutathione/glutathione disulfide (GSH/GSSG) ratio significantly increased. The levels of malondialdehyde (MDA), intracellular reactive oxygen species (ROS), tumor necrosis factor-α(TNF-α), and interleukin-6 (IL-6) decreased in astragalin-treated groups. The infarct size (IS) and apoptosis rate in hearts from astragalin-treated groups were lower than those in hearts from the I/R group. Western blot analysis also revealed that astragalin preconditioning significantly reduced Bax level, whereas Bcl-2 was increased in the myocardium. Therefore, astragalin exhibited cardioprotective effects via its antioxidative, antiapoptotic, and anti-inflammatory activities.

scholarly journals Protective Effects ofElaeagnus angustifoliaLeaf Extract against Myocardial Ischemia/Reperfusion Injury in Isolated Rat Heart

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Binsheng Wang ◽  
Hengyi Qu ◽  
Jun Ma ◽  
Xiling Sun ◽  
Dong Wang ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Aqueous Extract ◽  
Rat Heart ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Isolated Rat Heart ◽  
Protective Effects ◽  
Elaeagnus Angustifolia ◽  
Myocardial Ischemia Reperfusion ◽  
Isolated Rat

The purpose of this study is to clarify the cardioprotective property of the aqueous extract ofElaeagnus angustifoliaL. leaf (EA) against myocardial ischemia/reperfusion injury in isolated rat heart. The myocardial ischemia/reperfusion (I/R) injury model of isolated rat heart was set up by the use of improved Langendorff retrograde perfusion technology. Compared with the ischemia/reperfusion (I/R) group, the aqueous extract ofElaeagnus angustifoliaL. leaf (0.5 mg/mL, 1.0 mg/mL) pretreatment markedly improved the coronary flow (CF) and raised left ventricular developed pressure (LVDP) and maximum rise/down velocity (±dp/dtmax). The infarct size of the EA-treated hearts was smaller than that of I/R group. After treatment with EA, the superoxide dismutase (SOD) activity increased; malondialdehyde (MDA) and protein carbonyl content reduced more obviously (P<0.01) than that of I/R injury myocardial tissue.Conclusion. Results from the present study showed that the aqueous extract ofElaeagnus angustifoliaL. leaf has obvious protective effects on myocardial I/R injury, which may be related to the improvement of myocardial oxidative stress states.

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