Ferulic Acid Supplementation Increases Lifespan and Stress Resistance via Insulin/IGF-1 Signaling Pathway in C. elegans

• Published in: International journal of molecular sciences Vol. 22; no. 8; p. 4279
• Main Authors: Li, Hui, Yu, Xiaoxuan, Meng, Fanwei, Zhao, Zhenyu, Guan, Shuwen, Wang, Liping
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 20-04-2021; MDPI
• Subjects: Acids; Aging; Alzheimer's disease; Animals; Antioxidants; Autophagy; Caenorhabditis elegans; Caenorhabditis elegans Proteins - genetics; Caenorhabditis elegans Proteins - metabolism; Coumaric Acids - administration & dosage; Dietary Supplements; DNA-Binding Proteins; Ferulic acid; Food; Forkhead Transcription Factors - metabolism; Free radicals; Gene Expression Profiling; Genome-Wide Association Study; Insulin; Insulin - metabolism; Insulin-like growth factor I; Insulin-Like Growth Factor I - metabolism; insulin/IGF-1; Life span; lifespan; Locomotion; Longevity; Mammals; Mitochondria; Models, Biological; Mutants; Nematodes; Oxidation resistance; Oxidative stress; Oxidative Stress - drug effects; Physiology; Polyglutamine; Reactive Oxygen Species - metabolism; Signal Transduction; stress resistant; Stress, Physiological; Transcription factors; Transcription Factors - genetics; Transcription Factors - metabolism; Worms; Caenorhabditis elegans; ferulic acid; stress resistant; insulin/IGF-1; lifespan
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms22084279

Ferulic acid (FA) is a naturally-occurring well-known potent antioxidant and free radical scavenger. FA supplementation is an effective strategy to delay aging, but the underlying mechanism remains unknown. In the present study, we examined the effects of FA on lifespan extension and its mechanism of FA in
(
). Results suggested that FA increased the lifespan of
, rather than altering the growth of
OP50. Meanwhile, FA promoted the healthspan of
by improving locomotion and reducing fat accumulation and polyQ aggregation. FA increased the resistance to heat and oxidative stress through reducing ROS. The upregulating of the expression of the
,
, and
were involved in the FA-mediated lifespan extension. Furthermore, FA treatment had no impact on the lifespan of
,
,
, and
mutants, confirming that insulin/IGF-1 signaling pathway and multiple longevity mechanisms were associated with the longevity mechanism of FA. We further found that mitochondrial signaling pathway was modulation involved in FA-mediated lifespan extension. With the results from RNA-seq results and mutants lifespan assay. These findings contribute to our knowledge of the lifespan extension and underlying mechanism of action of FA in
.