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Inhibition of Ultraviolet‐B Radiation Induced Photodamage by Trigonelline Through Modulation of Mitogen Activating Protein Kinases and Nuclear Factor‐κB Signaling Axis in Skin
Author(s) -
A. Nazir Lone,
Tanveer Malik A.,
Umar Sheikh A.,
Love Sharma,
Divya Gupta,
Tasduq Sheikh A.
Publication year - 2021
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/php.13369
Subject(s) - photoaging , phototoxicity , oxidative stress , chemistry , human skin , lipid peroxidation , reactive oxygen species , skin aging , photoprotection , apoptosis , microbiology and biotechnology , cancer research , in vitro , biochemistry , biology , medicine , dermatology , photosynthesis , genetics
Cutaneous photodamage is incited via exposure of ultraviolet‐B (UV‐B) radiation to skin, characterized by the manifestation of oxidative stress, inflammation, collagen degradation and apoptosis which translates to external aging signs such as wrinkle formation and leathery skin appearance. Meanwhile, it increases cellular susceptibility to photocarcinogenesis. Several studies have accumulated evidence regarding the usage of natural agents in reversing the clinical signs of photoaging as well as preventing photo‐toxicity at molecular level. In this study, we have explored the therapeutic potential of natural agent Trigonelline (TG) against UV‐B radiation mediated skin photodamage. Various parameters modulated by the exposure of UV‐B radiation were investigated in human skin cells and chronic photodamage mice model (Balb/c). We found that TG alleviates UV‐B radiation induced photodamage in human skin cells and Balb/c skin mice. TG treatment in UV‐B irradiated skin cells abates UV‐B radiation mediated phototoxicity, oxidative stress, inflammation and apoptosis. At molecular level, we observed TG treatment significantly prevents the reactive oxygen species (ROS) generation and lipid peroxidation, restores collagen synthesis and matrix metalloproteinase (MMPs) levels. The in vitro findings were replicated in the in vivo model. We found that the TG acts potentially via modulation of ROS‐MAPKs‐NF‐κB axis. Collectively, we propose that TG acts antagonistically against UV‐B mediated skin damage and has strong potential to be developed as a therapeutic and cosmetical agent against photodamage disorders.