Abstract
The need for clinical remedies to the multiple age-related deficiencies in skin
function brought on by extrinsic and intrinsic causes is increased by these
demographic changes. Reactive oxygen species (ROS), mitochondrial
deoxyribonucleic acid (mtDNA) mutations, telomere shortening, as well as other
factors, contribute to the aging of the skin. In this overview, the issue of
human skin aging is introduced, along with several pathways and the protective
effects of ferulic acid in light of current patents. The complex antioxidant
effect of ferulic acid depends on the “sweeping” away of free
radicals as well as the suppression of the synthesis of ROS or nitrogen.
Furthermore, Cu (II) or Fe protonated metal ions are chelated by this acid (II).
Ferulic acid is a free radical scavenger as well as an enzyme inhibitor,
increasing the activity of enzymes that scavenge free radicals while decreasing
the activity of enzymes that speed up the creation of free radicals. AMPK
signalling, which can regulate cellular homeostasis, stress tolerance, cell
survival and proliferation, cell death, and autophagy, has recently been linked
to aging and lifespan. Therefore, Caenorhabditis elegans (C. elegans) and
rodents had longer life-spans due to specific AMPK activation. By inhibiting the
TGF-β/Smad signalling pathway, UV irradiation can reduce the
production of procollagen. Glycation changes the skin’s physical
characteristics, making it less elastic and stiffer. . Excessive free radicals
simultaneously trigger the nuclear factor kappa B (NF- κB) signalling
pathway, increasing TNF levels and matrix metalloproteinase production
(MMPs).
Key words
AMPK signalling - NF-κB signaling - aging - reactive oxygen species - ferulic acid
