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Dipeptidyl peptidase (DPP)-4 inhibitor exerts cardioprotective effects. However, its benefits during cardiac ischemia-reperfusion (IR) injury are not clear. We hypothesized that 1) DPP-4 inhibitor reduces fatal arrhythmias, cardiac dysfunction, and infarct size during IR, and 2) this cardioprotection is via attenuating cardiac mitochondrial dysfunction and cellular apoptosis.
Rats were randomized to receive either DPP-4 inhibitor (vildagliptin, Vil) 2.0 mg/kg or normal saline solution (NSS) intravenously (n=5/ group) prior to a 30-min left anterior descending coronary artery occlusion, followed by a 120-min reperfusion. Arrhythmia scores, cardiac functions, and the infarct size were evaluated. Cardiac tissues were harvested for mitochondria and immunoblot study.
Compared to control, DPP-4 inhibitor significantly reduced infarct size (44% reduction, Figure) and preserved systolic function, while arrhythmia scores were not different. Vildagliptin significantly increased Bcl-2 and pro-caspase3 expression, whereas p-connexin43/total connexin43 ratio was not different. In cardiac mitochondria, DPP-4 inhibitor significantly reduced the reactive oxygen species (ROS) production, mitochondrial swelling, and mitochondrial depolarization (Figure).
DPP-4 inhibitor provides cardioprotection during IR by reducing infarct size and improving systolic dysfunction by attenuating cardiac mitochondrial dysfunction and apoptosis.
Poster Sessions, Expo North
Monday, March 11, 2013, 9:45 a.m.-10:30 a.m.
Session Title: ACS Therapy: Basic and Translational
Abstract Category: 3. Acute Coronary Syndromes: Therapy
Presentation Number: 1301-186
- 2013 American College of Cardiology Foundation