Key result
Oral apigenin supplementation reversed vascular endothelial dysfunction and large elastic artery stiffening, and prevented foam cell formation in preclinical models of aging.
Why the study?
Does oral apigenin supplementation improve arterial dysfunction and reduce vascular inflammation in preclinical models of aging?
Does oral apigenin supplementation improve arterial dysfunction and reduce vascular inflammation in preclinical models of aging?
Preclinical evidence suggests oral apigenin supplementation improves age-related arterial dysfunction and vascular inflammation, providing a basis for future translational studies.
Hypothesis-generating in aged animal models; does not support clinical use and leaves open need for human trials.
Our study provides novel evidence that oral apigenin supplementation can reverse two clinically important indicators of arterial dysfunction with age, namely, vascular endothelial dysfunction and large elastic artery stiffening, and prevents foam cell formation in an established cell culture model of early atherosclerosis. Importantly, our results provide extensive insight into the biological mechanisms of apigenin action, including increased nitric oxide bioavailability, normalization of age-related increases in arterial ROS production and oxidative stress, reversal of age-associated aortic intrinsic mechanical wall stiffening and adverse remodeling of the extracellular matrix, and suppression of vascular inflammation. Given that apigenin is commercially available as a dietary supplement in humans, these preclinical findings provide the experimental basis for future translational studies assessing the potential of apigenin to treat arterial dysfunction and reduce cardiovascular disease risk with aging.
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Clayton et al. (2021) studied Arterial dysfunction with aging. Oral apigenin supplementation was evaluated on Vascular endothelial dysfunction and large elastic artery stiffening. Oral apigenin supplementation reversed vascular endothelial dysfunction and large elastic artery stiffening, and prevented foam cell formation in preclinical models of aging.
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