The cardioprotective effects of (-)-Epicatechin are mediated through arginase activity inhibition in a murine model of ischemia/reperfusion

Pilar Ortiz-Vilchis, Miguel Ortiz-Flores, Marcela Pacheco, Israel Ramirez-Sanchez, Aldo Moreno-Ulloa, Lourdes Vega, Alicia Ortiz, Francisco Villarreal, Ivan Rubio-Gayosso, Nayelli Najera, Eduardo Meaney, Guillermo Ceballos

Resultado de la investigación: Contribución a una revistaArtículorevisión exhaustiva

10 Citas (Scopus)

Resumen

The production of nitric oxide (NO) by nitric oxide synthases (NOS) depends on the bioavailability of L-arginine as NOS competes with arginase for this common substrate. As arginase activity increases, less NO is produced and adverse cardiovascular consequences can emerge. (-)-Epicatechin (EPI), the most abundant flavonoid in cacao, has been reported to stimulate endothelial and neuronal NOS expression and function leading to enhanced vascular function and cardioprotective effects. However, little is known about the effects of EPI on myocardial arginase activity. The aim of the present study was to determine if EPI is able to interact and modulate myocardial arginase and NOS expression and activity. For this purpose, in silico modeling, in vitro activity assays and a rat model of ischemia/reperfusion injury were used. In silico and in vitro results demonstrate that EPI can interact with arginase and significantly decrease its activity. In vivo, 10 days of EPI pretreatment reduces ischemic myocardium arginase expression while increasing NOS expression and phosphorylation levels. Altogether, these results may partially account for the cardioprotective effects of EPI.

Idioma originalInglés
Páginas (desde-hasta)335-342
Número de páginas8
PublicaciónEuropean Journal of Pharmacology
Volumen818
DOI
EstadoPublicada - 5 ene 2018

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