• Mariuxi C Manukyan, Collin H Alvernaz, Jeffrey A Poynter, Yue Wang, Benjamin D Brewster, Brent R Weil, Aaron M Abarbanell, Jeremy L Herrmann, Brandon J Crowe, Andrew C Keck, and Daniel R Meldrum.
• Department of Surgery, Indiana University School of Medicine, Indianapolis, IN, USA.
• Surgery. 2011 Aug 1;150(2):231-9.

BackgroundCardiac surgery induces the release of inflammatory mediators that can prolong cardiac dysfunction after operative intervention. Interleukin-10 (IL-10), a potent inhibitor of myocardial inflammation, is a known factor in myocardial protection after ischemia/reperfusion (I/R) injury. We hypothesized that IL-10 activity during initial reperfusion is mediated through the signal transducer and activator of transcription 3 (STAT3) pathway.MethodsAdult rat hearts were isolated and perfused via Langendorff protocol and subjected to global I/R. After determining the effective IL-10 dose, hearts were administered vehicle, IL-10, or IL-10 + Stattic (specific STAT3 inhibitor) 1 min prior to ischemia. After reperfusion, hearts were sectioned and assessed for levels of myocardial inflammatory cytokines and protein.ResultsThe IL-10 minimum effective dose was 1 μg. IL-10-treated hearts had improved markedly myocardial function after global I/R compared to both vehicle and IL-10 + Stattic groups. In addition, IL-10 treatment was associated with a significant decrease in myocardial interleukin-1β (IL-1β) and interleukin-6 (IL-6) and increase in myocardial IL-10. Myocardial STAT3 was elevated markedly in IL-10 treated hearts.ConclusionIL-10 improves myocardial function after acute global I/R and suppresses inflammation through the STAT3 pathway. The administration of anti-inflammatory agents may have potential therapeutic applications in cardiac surgery.Copyright © 2011 Mosby, Inc. All rights reserved.

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