Fenofibrate plus Metformin Produces Cardioprotection in a Type 2 Diabetes and Acute Myocardial Infarction ModelReportar como inadecuado

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PPAR Research - Volume 2016 2016, Article ID 8237264, 14 pages -

Research Article

Department of Pharmacobiology, Research and Advanced Studies Center, National Polytechnic Institute IPN, Calzada de los Tenorios No. 235, Colonia Granjas Coapa, Tlalpan, 14330 Mexico City, Mexico

Department of Pharmacology, National Institute of Cardiology Ignacio Chávez, Juan Badiano No. 1, Colonia Sección XVI, Tlalpan, 14080 Mexico City, Mexico

Department of Neurochemistry, National Institute of Neurology and Neurosurgery Manuel Velasco Suárez, Insurgentes Sur No. 3877, Colonia La Fama, Tlalpan, 14269 Mexico City, Mexico

Received 7 January 2016; Accepted 18 February 2016

Academic Editor: Yanbo Fan

Copyright © 2016 Víctor Hugo Oidor-Chan et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


We investigated whether fenofibrate, metformin, and their combination generate cardioprotection in a rat model of type 2 diabetes T2D and acute myocardial infarction AMI. Streptozotocin-induced diabetic- DB- rats received 14 days of either vehicle, fenofibrate, metformin, or their combination and immediately after underwent myocardial ischemia-reperfusion I-R. Fenofibrate plus metformin generated cardioprotection in a DBI-R model, reported as decreased coronary vascular resistance, compared to DBI-R-Vehicle, smaller infarct size, and increased cardiac work. The subchronic treatment with fenofibrate plus metformin increased, compared with DBI-R-Vehicle, total antioxidant capacity, manganese-dependent superoxide dismutase activity MnSOD, guanosine triphosphate cyclohydrolase I GTPCH-I expression, tetrahydrobiopterin : dihydrobiopterin BH4 : BH2 ratio, endothelial nitric oxide synthase eNOS activity, nitric oxide NO bioavailability, and decreased inducible NOS iNOS activity. These findings suggest that PPARα activation by fenofibrate + metformin, at low doses, generates cardioprotection in a rat model of T2D and AMI and may represent a novel treatment strategy to limit I-R injury in patients with T2D.

Autor: Víctor Hugo Oidor-Chan, Enrique Hong, Francisca Pérez-Severiano, Sergio Montes, Juan Carlos Torres-Narváez, Leonardo del V

Fuente: https://www.hindawi.com/


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