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- Title
Disparate Effects of Stilbenoid Polyphenols on Hypertrophic Cardiomyocytes In Vitro vs. in the Spontaneously Hypertensive Heart Failure Rat.
- Authors
Akinwumi, Bolanle C.; Raj, Pema; Lee, Danielle I.; Acosta, Crystal; Liping Yu; Thomas, Samuel M.; Nagabhushanam, Kalyanam; Majeed, Muhammed; Davies, Neal M.; Netticadan, Thomas; Anderson, Hope D.
- Abstract
Stilbenoids are bioactive polyphenols, and resveratrol (trans-3,5,40-trihydroxystilbene) is a representative stilbenoid that reportedly exerts cardioprotective actions. As resveratrol exhibits low oral bioavailability, we turned our attention to other stilbenoid compounds with a history of medicinal use and/or improved bioavailability. We determined the effects of gnetol (trans-3,5,2′,6′-tetrahydroxystilbene) and pterostilbene (trans-3,5-dimethoxy-4′-hydroxystilbene) on cardiac hypertrophy. In vitro, gnetol and pterostilbene prevented endothelin-1-induced indicators of cardiomyocyte hypertrophy including cell enlargement and protein synthesis. Gnetol and pterostilbene stimulated AMP-activated protein kinase (AMPK), and inhibition of AMPK, using compound C or shRNA knockdown, abolished these anti-hypertrophic effects. In contrast, resveratrol, gnetol, nor pterostilbene reduced blood pressure or hypertrophy in the spontaneously hypertensive heart failure (SHHF) rat. In fact, AMPK levels were similar between Sprague-Dawley and SHHF rats whether treated by stilbenoids or not. These data suggest that the anti-hypertrophic actions of resveratrol (and other stilbenoids?) do not extend to the SHHF rat, which models heart failure superimposed on hypertension. Notably, SHHF rat hearts exhibited prolonged isovolumic relaxation time (an indicator of diastolic dysfunction), and this was improved by stilbenoid treatment. In conclusion, stilbenoid-based treatment as a viable strategy to prevent pathological cardiac hypertrophy, a major risk factor for heart failure, may be context-dependent and requires further study.
- Subjects
CARDIAC hypertrophy; POLYPHENOLS; HEART cells; BIOACTIVE compounds; PREPROENDOTHELIN; HEART failure risk factors; PREVENTION; THERAPEUTICS
- Publication
Molecules, 2017, Vol 22, Issue 2, p204
- ISSN
1420-3049
- Publication type
Article
- DOI
10.3390/molecules22020204