Cardiac fibrosis is one of the hallmarks of a diabetic cardiomyopathy. When activated, cardiac fibroblasts (CFs) increase the production of extracellular matrix proteins. Transforming growth factor (TGF)-β1 is known to mediate cardiac fibrosis through the SMAD pathway. High glucose (HG = 25mM) cell culture media can activate CFs using TGF-β1. There is a need to identify effective antifibrotic agents. Studies in animals indicate that treatment with (-)-epicatechin (Epi) appears capable of reducing myocardial fibrosis. Epi binds to G-protein coupled estrogen receptor (GPER) and activates downstream pathways. We evaluated the potential of Epi to mitigate the development of a profibrotic phenotype in HG stimulated CFs. CF primary cultures were isolated from young male rats and were exposed for up to 48h HG media and treated with vehicle or 1 μM Epi. Relevant profibrotic end points were measured by the use of various biochemical assays. HG exposure...
Antifibrotic effects of (-)-epicatechin on high glucose stimulated cardiac fibroblasts.
F. Villarreal, Department of Medicine, School of Medicine, University of California, San Diego, 9500 Gilman Drive BSB4028, La Jolla, CA 92093-0613J, USA. E-mail email@example.com
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Garate-Carrillo, A., Ramirez-Sanchez, I., Nguyen, J., Gonzalez, J., Ceballos, G., Villarreal, F.; Antifibrotic effects of (-)-epicatechin on high glucose stimulated cardiac fibroblasts.. IFIS Food and Health Sciences Database 2022; doi:
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