• Something wrong with this record ?

Liraglutide preserves intracellular calcium handling in isolated murine myocytes exposed to oxidative stress

S. Palee, SC. Chattipakorn, N. Chattipakorn

. 2017 ; 66 (5) : 889-895. [pub] 20170718

Language English Country Czech Republic

Document type Journal Article

Persistent link   https://www.medvik.cz/link/bmc18026971

In ischemic/reperfusion (I/R) injured hearts, severe oxidative stress occurs and is associated with intracellular calcium (Ca(2+)) overload. Glucagon-Like Peptide-1 (GLP-1) analogues have been shown to exert cardioprotection in I/R heart. However, there is little information regarding the effects of GLP-1 analogue on the intracellular Ca(2+) regulation in the presence of oxidative stress. Therefore, we investigated the effects of GLP-1 analogue, (liraglutide, 10 microM) applied before or after hydrogen peroxide (H(2)O(2), 50 microM) treatment on intracellular Ca(2+) regulation in isolated cardiomyocytes. We hypothesized that liraglutide can attenuate intracellular Ca(2+) overload in cardiomyocytes under H(2)O(2)-induced cardiomyocyte injury. Cardiomyocytes were isolated from the hearts of male Wistar rats. Isolated cardiomyocytes were loaded with Fura-2/AM and fluorescence intensity was recorded. Intracellular Ca(2+) transient decay rate, intracellular Ca(2+) transient amplitude and intracellular diastolic Ca(2+) levels were recorded before and after treatment with liraglutide. In H(2)O(2) induced severe oxidative stressed cardiomyocytes (which mimic cardiac I/R) injury, liraglutide given prior to or after H(2)O(2) administration effectively increased both intracellular Ca(2+) transient amplitude and intracellular Ca(2+) transient decay rate, without altering the intracellular diastolic Ca(2+) level. Liraglutide attenuated intracellular Ca(2+) overload in H(2)O(2)-induced cardiomyocyte injury and may be responsible for cardioprotection during cardiac I/R injury by preserving physiological levels of calcium handling during the systolic and diastolic phases of myocyte activation.

References provided by Crossref.org

000      
00000naa a2200000 a 4500
001      
bmc18026971
003      
CZ-PrNML
005      
20180815074342.0
007      
ta
008      
180730s2017 xr d f 000 0|eng||
009      
AR
024    7_
$a 10.33549/physiolres.933558 $2 doi
035    __
$a (PubMed)28730832
040    __
$a ABA008 $b cze $d ABA008 $e AACR2
041    0_
$a eng
044    __
$a xr
100    1_
$a Palee, S. $u Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand; Center of Excellence in Cardiac Electrophysiology, Chiang Mai University, Chiang Mai, Thailand
245    10
$a Liraglutide preserves intracellular calcium handling in isolated murine myocytes exposed to oxidative stress / $c S. Palee, SC. Chattipakorn, N. Chattipakorn
520    9_
$a In ischemic/reperfusion (I/R) injured hearts, severe oxidative stress occurs and is associated with intracellular calcium (Ca(2+)) overload. Glucagon-Like Peptide-1 (GLP-1) analogues have been shown to exert cardioprotection in I/R heart. However, there is little information regarding the effects of GLP-1 analogue on the intracellular Ca(2+) regulation in the presence of oxidative stress. Therefore, we investigated the effects of GLP-1 analogue, (liraglutide, 10 microM) applied before or after hydrogen peroxide (H(2)O(2), 50 microM) treatment on intracellular Ca(2+) regulation in isolated cardiomyocytes. We hypothesized that liraglutide can attenuate intracellular Ca(2+) overload in cardiomyocytes under H(2)O(2)-induced cardiomyocyte injury. Cardiomyocytes were isolated from the hearts of male Wistar rats. Isolated cardiomyocytes were loaded with Fura-2/AM and fluorescence intensity was recorded. Intracellular Ca(2+) transient decay rate, intracellular Ca(2+) transient amplitude and intracellular diastolic Ca(2+) levels were recorded before and after treatment with liraglutide. In H(2)O(2) induced severe oxidative stressed cardiomyocytes (which mimic cardiac I/R) injury, liraglutide given prior to or after H(2)O(2) administration effectively increased both intracellular Ca(2+) transient amplitude and intracellular Ca(2+) transient decay rate, without altering the intracellular diastolic Ca(2+) level. Liraglutide attenuated intracellular Ca(2+) overload in H(2)O(2)-induced cardiomyocyte injury and may be responsible for cardioprotection during cardiac I/R injury by preserving physiological levels of calcium handling during the systolic and diastolic phases of myocyte activation.
650    _2
$a zvířata $7 D000818
650    _2
$a vápníková signalizace $x účinky léků $x fyziologie $7 D020013
650    _2
$a kultivované buňky $7 D002478
650    _2
$a peroxid vodíku $x toxicita $7 D006861
650    _2
$a hypoglykemika $x farmakologie $7 D007004
650    _2
$a intracelulární tekutina $x účinky léků $x metabolismus $7 D007424
650    _2
$a liraglutid $x farmakologie $7 D000069450
650    _2
$a mužské pohlaví $7 D008297
650    _2
$a kardiomyocyty $x účinky léků $x metabolismus $7 D032383
650    _2
$a oxidační stres $x účinky léků $x fyziologie $7 D018384
650    _2
$a krysa rodu Rattus $7 D051381
650    _2
$a potkani Wistar $7 D017208
655    _2
$a časopisecké články $7 D016428
700    1_
$a Chattipakorn, S. C. $u Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand; Center of Excellence in Cardiac Electrophysiology, Chiang Mai University, Chiang Mai, Thailand; Department of Oral Biology and Diagnostic Science, Faculty of Dentistry, Chiang Mai University, Chiang Mai, Thailand
700    1_
$a Chattipakorn, N. $u Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand; Cardiac Electrophysiology Unit, Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand; Center of Excellence in Cardiac Electrophysiology, Chiang Mai University, Chiang Mai, Thailand
773    0_
$w MED00003824 $t Physiological research $x 1802-9973 $g Roč. 66, č. 5 (2017), s. 889-895
856    41
$u https://pubmed.ncbi.nlm.nih.gov/28730832 $y Pubmed
910    __
$a ABA008 $b A 4120 $c 266 $y 4 $z 0
990    __
$a 20180730 $b ABA008
991    __
$a 20180810135758 $b ABA008
999    __
$a ok $b bmc $g 1326182 $s 1023903
BAS    __
$a 3
BAS    __
$a PreBMC
BMC    __
$a 2017 $b 66 $c 5 $d 889-895 $e 20170718 $i 1802-9973 $m Physiological research $n Physiol. Res. (Print) $x MED00003824
LZP    __
$b NLK118 $a Pubmed-20180730
Back

Find record

Citation metrics

Archiving options