Senolytic effects of a modified Gingerenone A.

Ruin Moaddel, Chad Sanehira, Gregory Keyes, Chang-Yi Cui, Reza Ahmadkhania, Julián Candia, Nathan L Price, Sarah Eckroth, Bryce Middleton, Mohammed Khadeer, Caio H Mazucanti, Ross A McDevitt, Myriam Gorospe, Rafael de Cabo, Josephine M Egan, Christopher E Ramsden, Luigi Ferrucci

Laboratory of Clinical Investigation, National Institute on Aging, Intramural Research Program, NIH, Baltimore, MD, USA. [email protected] of Clinical Investigation, National Institute on Aging, Intramural Research Program, NIH, Baltimore, MD, USA. [email protected]. · pubmed

Paper

Abstract

Senescent cells accumulate with aging and are associated with several age-associated diseases and functional declines. Eliminating senescent cells with senolytics improves aging phenotypes in mouse models and may improve the health of people with chronic diseases. To date, very few senotherapeutic (senolytics and senomorphics) compounds have been identified. In a recent study, we reported that gingerenone A (GinA) has a senolytic effect via mechanisms including the activation of caspase-3 activity and apoptotic cell death. In this study, we investigated whether GinA has senotherapeutic properties in a mouse model of senescence. Moreover, we modified GinA with eicosapentaenoic acid (EPA) esters (GinA-EPA) or docosahexaenoic acid (DHA) esters (GinA-DHA) to generate modified gingerenone A (modGinA) that could enhance GinA effects. We found that both GinA and modGinA induced biochemical and histological changes consistent with anti-inflammatory, senolytic, and senomorphic effects, leading to improved metabolic and mitochondrial functions.

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Research summary

Modified gingerenone A exhibits senolytic effects that may improve metabolic and mitochondrial functions in a mouse model of senescence. The study addresses the accumulation of senescent cells, which is a root cause of aging and age-related diseases, making it relevant to longevity research.

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