Chrysin preserves renal structure and mitochondrial quality control in D-galactose-induced kidney aging: enhanced...

Aging-associated renal dysfunction is driven by mitochondrial impairment, oxidative stress, inflammation, and apoptosis. This study investigated the renoprotective effects of chrysin (Chry) and nano-encapsulated chrysin (Chry-Cas-NPs) in a D-galactose-induced rat model of kidney aging, with emphasis on mitochondrial quality control mechanisms.

Sixty male Wistar rats were assigned to control, D-galactose, Chry, and Chry-Cas-NPs groups and treated for 10 weeks. Renal function indices, mitochondrial respiratory chain activities, ATP levels, mitophagy-related proteins (PINK1/Parkin), mitochondrial gene expression, oxidative stress markers, inflammatory mediators, apoptotic proteins, and renal histopathology were evaluated.

D-galactose induced marked renal dysfunction, tubular and glomerular degeneration, and mitochondrial structural damage. These changes were associated with impaired respiratory chain activity, reduced ATP production, altered PINK1/Parkin expression, downregulation of mitochondrial genes, increased oxidative stress (reactive oxygen species, malondialdehyde), depletion of antioxidant defenses, increased MAPK and NF-κB/TLR4 signaling, elevated pro-inflammatory cytokines, and enhanced apoptosis. Chry partially improved these alterations. Notably, Chry-Cas-NPs significantly restored mitochondrial function and structure, modulated PINK1/Parkin-related protein expression, attenuated oxidative and inflammatory responses, reduced apoptosis, and preserved renal architecture more effectively than free Chry.

Chry-Cas-NPs provided greater renoprotective effects than free Chry, associated with preservation of mitochondrial function and modulation of PINK1/Parkin-related proteins, oxidative stress, inflammation, and apoptosis in experimental renal aging.