open access

Vol 20, No 6 (2013)
Original articles
Published online: 2013-12-11
Get Citation

Exendin-4 attenuates myocardial ischemia and reperfusion injury by inhibiting high mobility group box 1 protein expression

Gangying Hu, Yijie Zhang, Hong Jiang, Xiaorong Hu
DOI: 10.5603/CJ.2013.0159
·
Cardiol J 2013;20(6):600-604.

open access

Vol 20, No 6 (2013)
Original articles
Published online: 2013-12-11

Abstract

Background: High mobility group box 1 protein (HMGB1) plays an important role in myocardial ischemia and reperfusion (I/R) injury. Exendin-4 (Ex-4), glucagon-like peptide-1 receptor agonist, has been reported to attenuate myocardial I/R injury. This study was to investigate the potential mechanism by which Ex-4 attenuates myocardial I/R injury in rats.

Methods: Anesthetized male rats were once treated with Ex-4 (5 μg/kg, i.v.) 1 h before ischemiain the absence and/or presence of exendin (9-39) (an antagonist for glucagon-like peptide-1receptor, 5 μg/kg, i.v.), and then subjected to ischemia for 30 min followed by reperfusion for 4 h. Lactate dehydrogenase (LDH), creatine kinase (CK), malondialdehyde (MDA), superoxide dismutase (SOD) activity and infarct size were measured. HMGB1 expression was assessed by immunoblotting.

Results: The results showed that pretreatment of Ex-4 could significantly decrease the infarct size and the levels of LDH and CK after 4 h reperfusion (all p < 0.05). Ex-4 could also significantly inhibit the increase of the MDA level, the decrease of the SOD level (both p < 0.05). Meanwhile, Ex-4 could signifi cantly inhibit HMGB1 expression induced by I/R. Administration of exendin (9-39) could abolish the protective effect of Ex-4 (all p < 0.05).

Conclusions: The present study suggested that Ex-4 could attenuate myocardial I/R injury which may be associated with inhibiting HMGB1 expression.

Abstract

Background: High mobility group box 1 protein (HMGB1) plays an important role in myocardial ischemia and reperfusion (I/R) injury. Exendin-4 (Ex-4), glucagon-like peptide-1 receptor agonist, has been reported to attenuate myocardial I/R injury. This study was to investigate the potential mechanism by which Ex-4 attenuates myocardial I/R injury in rats.

Methods: Anesthetized male rats were once treated with Ex-4 (5 μg/kg, i.v.) 1 h before ischemiain the absence and/or presence of exendin (9-39) (an antagonist for glucagon-like peptide-1receptor, 5 μg/kg, i.v.), and then subjected to ischemia for 30 min followed by reperfusion for 4 h. Lactate dehydrogenase (LDH), creatine kinase (CK), malondialdehyde (MDA), superoxide dismutase (SOD) activity and infarct size were measured. HMGB1 expression was assessed by immunoblotting.

Results: The results showed that pretreatment of Ex-4 could significantly decrease the infarct size and the levels of LDH and CK after 4 h reperfusion (all p < 0.05). Ex-4 could also significantly inhibit the increase of the MDA level, the decrease of the SOD level (both p < 0.05). Meanwhile, Ex-4 could signifi cantly inhibit HMGB1 expression induced by I/R. Administration of exendin (9-39) could abolish the protective effect of Ex-4 (all p < 0.05).

Conclusions: The present study suggested that Ex-4 could attenuate myocardial I/R injury which may be associated with inhibiting HMGB1 expression.

Get Citation

Keywords

exendin-4, myocardial ischemia, reperfusion, high mobility group box 1 protein

About this article
Title

Exendin-4 attenuates myocardial ischemia and reperfusion injury by inhibiting high mobility group box 1 protein expression

Journal

Cardiology Journal

Issue

Vol 20, No 6 (2013)

Pages

600-604

Published online

2013-12-11

DOI

10.5603/CJ.2013.0159

Bibliographic record

Cardiol J 2013;20(6):600-604.

Keywords

exendin-4
myocardial ischemia
reperfusion
high mobility group box 1 protein

Authors

Gangying Hu
Yijie Zhang
Hong Jiang
Xiaorong Hu

Important: This website uses cookies. More >>

The cookies allow us to identify your computer and find out details about your last visit. They remembering whether you've visited the site before, so that you remain logged in - or to help us work out how many new website visitors we get each month. Most internet browsers accept cookies automatically, but you can change the settings of your browser to erase cookies or prevent automatic acceptance if you prefer.

By "Via Medica sp. z o.o." sp.k., ul. Świętokrzyska 73, 80–180 Gdańsk, Poland
tel.:+48 58 320 94 94, fax:+48 58 320 94 60, e-mail: viamedica@viamedica.pl