Open AccessFlavonoids mitigate neurodegeneration in aged Caenorhabditis elegans by mitochondrial uncoupling
Author(s) -
Cho Injeong,
Song HyunOk,
Cho Jeong Hoon
Publication year - 2020
Publication title -
food science and nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.614
H-Index - 27
ISSN - 2048-7177
DOI - 10.1002/fsn3.1956
Subject(s) - neurodegeneration , caenorhabditis elegans , fisetin , mitophagy , biology , mitochondrion , antioxidant , pink1 , neuroprotection , parkin , microbiology and biotechnology , biochemistry , pharmacology , flavonoid , parkinson's disease , disease , medicine , apoptosis , autophagy , gene
Dietary supplementation of flavonoids has been shown to reduce the severity of neurodegenerative disorders such as dementia, Parkinson's disease, and Alzheimer's disease by their antioxidant effects. However, their low bioavailability in vivo raises the question of how much their antioxidant capacity actually contributes to the mitigating effects. The physicochemical properties of flavonoids suggest they could function as mitochondrial uncouplers. Moreover, mitochondrial uncoupling alleviated neurodegeneration in Caenorhabditis elegans during aging in previous research. Therefore, we investigated whether various flavonoids (fisetin, quercetin, apigenin, chrysin, catechin, and naringenin) could reduce neuronal defects by mitochondrial uncoupling in C. elegans . Both neuronal defects and mitochondrial membrane potential were reduced in aged worms in nearly all of the flavonoid treatments suggesting that flavonoids may reduce neurodegeneration in C. elegans . However, there was no significant reduction of neuronal defects in mitophagy‐deficient pink‐1/pdr‐1 double mutants under flavonoid treatments. These results suggest that flavonoids could function as mitochondrial uncouplers to mitigate neurodegeneration in aged C. elegans , possibly via a PINK1/Parkin mitophagy process.