Cyanidin chloride activates mitophagy to delay aging via PINK1/parkin pathway

Food-derived bioactive compounds are increasingly recognized as promising nutritional candidates for modulating aging-associated functional decline. Among them, anthocyanidins, a major class of polyphenolic pigments widely present in dark-colored fruits, vegetables, and grains, have attracted attention because of their antioxidant, anti-inflammatory, and metabolic regulatory activities. Cyanidin chloride is a representative food-derived anthocyanidin found in edible plants such as blueberries, blackberries, purple cabbage, and black rice. However, whether Cyanidin chloride influences lifespan and aging-associated physiological decline, and how it affects mitochondrial homeostasis, remain incompletely understood. In this study, Caenorhabditis elegans and naturally aging mice were used to evaluate the effects of Cyanidin chloride. Cyanidin chloride extended lifespan in Caenorhabditis elegans and improved selected age-associated physiological readouts, including locomotor activity, lipofuscin accumulation, fertility preservation, and proteotoxicity-associated paralysis. Genetic analyses showed that these effects were largely dependent on the PINK-1/PDR-1 axis and were accompanied by increased expression of downstream autophagy-related genes (bec-1, lgg-1, and lgg-2), reduced reactive oxygen species (ROS) accumulation, and increased adenosine triphosphate (ATP) production. In aging mice, Cyanidin chloride administration was associated with improved survival, increased PINK1/Parkin-related protein markers, partially reduced the expression of inflammatory-related factors, and enhanced antioxidant-related gene expression. These findings suggest that Cyanidin chloride activates PINK1/Parkin-mediated mitophagy to alleviate aging-associated decline, providing a mechanistic basis for future studies on cyanidin-rich foods and anthocyanidin-based nutritional strategies.