Dipeptidyl peptidase-4 inhibitor reduces infarct size and preserves cardiac function via mitochondrial protection in ischaemia-reperfusion rat heart

Aim: We hypothesized that dipeptidyl peptidase (DPP)-4 inhibitor (vildagliptin) reduces fatal arrhythmias, cardiac dysfunction and infarct size caused by ischaemiareperfusion (I/R) injury via its attenuation of cardiac mitochondrial dysfunction. Methods: In total, 26 rats were randomized to receive...

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Main Authors: Chinda K., Sanit J., Chattipakorn S., Chattipakorn N.
Format: Article
Language:English
Published: 2014
Online Access:http://www.scopus.com/inward/record.url?eid=2-s2.0-84894488315&partnerID=40&md5=27a42fe85ff4ba125c96739a0978391d
http://cmuir.cmu.ac.th/handle/6653943832/983
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spelling th-cmuir.6653943832-9832014-08-29T09:17:32Z Dipeptidyl peptidase-4 inhibitor reduces infarct size and preserves cardiac function via mitochondrial protection in ischaemia-reperfusion rat heart Chinda K. Sanit J. Chattipakorn S. Chattipakorn N. Aim: We hypothesized that dipeptidyl peptidase (DPP)-4 inhibitor (vildagliptin) reduces fatal arrhythmias, cardiac dysfunction and infarct size caused by ischaemiareperfusion (I/R) injury via its attenuation of cardiac mitochondrial dysfunction. Methods: In total, 26 rats were randomized to receive either 1 mL normal saline solution or 2.0 mg/kg vildagliptin intravenously (n = 13/group) 30 min prior to a 30-min left anterior descending coronary artery occlusion, followed by a 120-min reperfusion. Arrhythmia scores, cardiac functions, infarct size and mitochondrial function were evaluated. Results: Vildagliptin reduced the infarct size by 44% and mitigated cardiac dysfunction by preserving cardiac function without altering the incidence of cardiac arrhythmias. Vildagliptin increased expression of Bcl-2 and pro-caspase3 in the ischaemic area, whereas Bax and phosphorylated-connexin43/total-connexin43 were not altered. Vildagliptin attenuated cardiac mitochondrial dysfunction by reducing the reactive oxygen species level and mitochondrial swelling. Conclusions: DPP-4 inhibitor provides cardioprotection by reducing the infarct size and ameliorating cardiac dysfunction in I/R hearts by attenuating cardiac mitochondrial dysfunction and cardiomyocyte apoptosis. © 2013 The Author(s). 2014-08-29T09:17:32Z 2014-08-29T09:17:32Z 2014 Article 14791641 10.1177/1479164113516134 http://www.scopus.com/inward/record.url?eid=2-s2.0-84894488315&partnerID=40&md5=27a42fe85ff4ba125c96739a0978391d http://cmuir.cmu.ac.th/handle/6653943832/983 English
institution Chiang Mai University
building Chiang Mai University Library
country Thailand
collection CMU Intellectual Repository
language English
description Aim: We hypothesized that dipeptidyl peptidase (DPP)-4 inhibitor (vildagliptin) reduces fatal arrhythmias, cardiac dysfunction and infarct size caused by ischaemiareperfusion (I/R) injury via its attenuation of cardiac mitochondrial dysfunction. Methods: In total, 26 rats were randomized to receive either 1 mL normal saline solution or 2.0 mg/kg vildagliptin intravenously (n = 13/group) 30 min prior to a 30-min left anterior descending coronary artery occlusion, followed by a 120-min reperfusion. Arrhythmia scores, cardiac functions, infarct size and mitochondrial function were evaluated. Results: Vildagliptin reduced the infarct size by 44% and mitigated cardiac dysfunction by preserving cardiac function without altering the incidence of cardiac arrhythmias. Vildagliptin increased expression of Bcl-2 and pro-caspase3 in the ischaemic area, whereas Bax and phosphorylated-connexin43/total-connexin43 were not altered. Vildagliptin attenuated cardiac mitochondrial dysfunction by reducing the reactive oxygen species level and mitochondrial swelling. Conclusions: DPP-4 inhibitor provides cardioprotection by reducing the infarct size and ameliorating cardiac dysfunction in I/R hearts by attenuating cardiac mitochondrial dysfunction and cardiomyocyte apoptosis. © 2013 The Author(s).
format Article
author Chinda K.
Sanit J.
Chattipakorn S.
Chattipakorn N.
spellingShingle Chinda K.
Sanit J.
Chattipakorn S.
Chattipakorn N.
Dipeptidyl peptidase-4 inhibitor reduces infarct size and preserves cardiac function via mitochondrial protection in ischaemia-reperfusion rat heart
author_facet Chinda K.
Sanit J.
Chattipakorn S.
Chattipakorn N.
author_sort Chinda K.
title Dipeptidyl peptidase-4 inhibitor reduces infarct size and preserves cardiac function via mitochondrial protection in ischaemia-reperfusion rat heart
title_short Dipeptidyl peptidase-4 inhibitor reduces infarct size and preserves cardiac function via mitochondrial protection in ischaemia-reperfusion rat heart
title_full Dipeptidyl peptidase-4 inhibitor reduces infarct size and preserves cardiac function via mitochondrial protection in ischaemia-reperfusion rat heart
title_fullStr Dipeptidyl peptidase-4 inhibitor reduces infarct size and preserves cardiac function via mitochondrial protection in ischaemia-reperfusion rat heart
title_full_unstemmed Dipeptidyl peptidase-4 inhibitor reduces infarct size and preserves cardiac function via mitochondrial protection in ischaemia-reperfusion rat heart
title_sort dipeptidyl peptidase-4 inhibitor reduces infarct size and preserves cardiac function via mitochondrial protection in ischaemia-reperfusion rat heart
publishDate 2014
url http://www.scopus.com/inward/record.url?eid=2-s2.0-84894488315&partnerID=40&md5=27a42fe85ff4ba125c96739a0978391d
http://cmuir.cmu.ac.th/handle/6653943832/983
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