Indocyanine Green-001 (ICG-001) Attenuates Wnt/β-catenininduces Myocardial Injury Following Sepsis
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- 1Department of Pharmacology and Therapeutics, College of Medicine, University of Kufa, Kufa, Iraq.
Published in Journal of Pharmacology and Pharmacotherapeutics
Correspondence: Nasser Ghaly Yousif
Department of Pharmacology and Therapeutics, College of Medicine, University of Kufa, Kufa, Iraq.
Email: yousif_ghaly@yahoo.com
Copyright: © 2017 The Author(s). This is an open access article.
Published: Jan 1, 2017, Received: Nov 4, 2016, Accepted: Jan 27, 2017
Abstract
Objective: To investigate the mechanistic pathway of both indocyanine green (ICG)‑001 in attenuated endotoxemia‑induced cardiac depression through downregulation cardiac Wnt/ β‑catenin cell signaling. Materials and Methods: Adult (4–6 months) male Albino‑Webster mice, their weights ranged from 25 to 30 g, were pretreated with ICG‑001 i.p., following cecal ligation and puncture (CLP). Left ventricle (LV) function was assessed using a microcatheter system. Monocyte chemoattractant protein‑1 (MCP‑1) and cytokines mediators in plasma and myocardium were analyzed by enzyme‑linked immunosorbent assay. Further, the cardiac Wnt protein measured by quantitative real‑time polymerase chain reaction while β‑catenin analysis through Western blotting procedure. The pathological changes and cells injury in the myocardium were examined using hematoxylin and eosin staining. Results: CLP mice displayed worse LV function. The exaggerated cardiac depression in CLP mice was associated with higher levels of MCP‑1 and cytokines in plasma and myocardium together with greater cardiac levels of cardiac troponin‑I and Wnt/β‑catenin. Neutralization of sepsis by either ICG‑001resulted in improved LV function and reductions in inflammatory mediators. Conclusion: Taken together, these data showed that ICG‑001 improved LV function following sepsis through downregulation of Wnt/β‑catenin and serve as a potential mechanistic pathway ICG‑001 in therapeutic cardiac endotoxemia in animal model.
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