Key result
DHEA treatment in diabetic rats improved oxidative balance, minimized structural changes, and completely restored the contractility of isolated papillary muscle.
Why the study?
Does dehydroepiandrosterone (DHEA) prevent cardiac fibrosis and impaired contractile function in rats with streptozotocin-induced diabetes?
Population
Rats with streptozotocin-induced diabetes
Comparison
Dehydroepiandrosterone administered in the diet… vs Untreated streptozotocin-diabetic rats and…
Design
Preclinical
Follow-up
6 weeks
Authors
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DHEA merits testing in human diabetic cardiomyopathy trials; leaves open translation beyond rodent models.
Does dehydroepiandrosterone (DHEA) prevent cardiac fibrosis and impaired contractile function in rats with streptozotocin-induced diabetes?
In a rat model of diabetic cardiomyopathy, DHEA treatment minimized structural changes and restored cardiac muscle function by reducing oxidative stress and fibrosis.
Aragno et al. (2007) studied Diabetic cardiomyopathy. Dehydroepiandrosterone (DHEA) vs. Untreated streptozotocin-diabetic rats was evaluated on Oxidative balance, AGEs, AGE receptors, transcription factors, profibrogenic growth factors, structural changes, and contractile force. DHEA treatment in diabetic rats improved oxidative balance, minimized structural changes, and completely restored the contractility of isolated papillary muscle.
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