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Glucagon‐like peptide‐1 mitigates myocardial ischemia‐reperfusion injury, and is associated with differential chemokine expression
Author(s) -
Dokken Betsy B.,
DavisGorman Grace,
La Bonte Laura R.,
McDonagh Paul F.
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.793.5
Subject(s) - chemokine , ischemia , medicine , reperfusion injury , glucagon like peptide 1 , myocardial infarction , ischemic preconditioning , endocrinology , inflammation , pharmacology , cardiology , anesthesia , diabetes mellitus , type 2 diabetes
After myocardial infarction, restoration of blood flow is critical to survival, however, reperfusion causes an inflammatory response that exacerbates the injury. Glucagon‐like Peptide‐1 (GLP‐1) has protective effects, but it's mechanism is poorly understood. Earlier, we found that postconditioning with GLP‐1 decreased ischemia‐reperfusion injury (IRI) after experimental myocardial ischemia in vivo , which was associated with decreased neutrophil accumulation. In this study, Sprague Dawley rats underwent a 30 minute coronary occlusion. Recombinant human GLP‐1 (30 pmol/kg/min) or vehicle was then infused for 2 hours of reperfusion. To determine the mechanism by which GLP‐1 mitigates neutrophil‐mediated IRI, we analyzed the expression of chemokines in plasma taken from animals before ischemia and at R120 using a rat cytokine array kit (RayBiotech, Inc). We found that two chemokines were differentially expressed. β‐NGF almost doubled in response to IR; GLP‐1 treatment abolished this increase (pre‐ischemia 16.6 ± 0.5; IR 30.9 ± 0.9; IR + GLP‐1 17.5 ± 1.3, p< 0.05, n=5). MCP‐1 decreased in response to IR; GLP‐1 treatment attenuated the decrease (pre‐ischemia 61.4 ± 4.8; IR 27.3 ± 2.1; IR + GLP‐1 54.6 ± 6.2, p< 0.05, n=5). GLP‐1 postconditioning may mitigate myocardial IRI in part by regulating the expression of chemokines. Supported by the Arizona Sarver Heart Center and NIH HL 58859.