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Baicalin Protects Keratinocytes from Toll‐like Receptor‐4 Mediated DNA Damage and Inflammation Following Ultraviolet Irradiation
Author(s) -
Min Wei,
Ahmad Israr,
Chang Michelle E.,
Burns Erin M.,
Qian Qihong,
Yusuf Nabiha
Publication year - 2015
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.12505
Subject(s) - baicalin , dna damage , chemistry , tlr4 , reactive oxygen species , inflammation , trif , signal transduction , toll like receptor , microbiology and biotechnology , cancer research , receptor , biochemistry , biology , dna , immunology , innate immune system , high performance liquid chromatography , chromatography
UVB radiation contributes to both direct and indirect damage to the skin including the generation of free radicals and reactive oxygen species ( ROS ), inflammatory responses, immunosuppression and gene mutations, which can ultimately lead to photocarcinogenesis. A plant‐derived flavonoid, baicalin, has been shown to have antioxidant, anti‐inflammatory and free radical scavenging activities. Previous studies from our laboratory have shown that in murine skin, Toll‐like receptor‐4 ( TLR 4) enhanced both UVB ‐induced DNA damage and inflammation. The aim of this study was to investigate the efficacy of baicalin against TLR 4‐mediated processes in the murine keratinocyte PAM 212 cell line. Our results demonstrate that treating keratinocytes with baicalin both before and after UV radiation (100 mJ cm −2 ) significantly inhibited the level of intracellular ROS and decreased cyclobutane pyrimidine dimers and 8‐Oxo‐2′‐deoxyguanosine (8‐oxo‐ dG )—markers of DNA damage. Furthermore, cells treated with baicalin demonstrated an inhibition of TLR 4 and its downstream signaling molecules, M y D 88, TRIF , TRAF 6 and IRAK 4. TLR 4 pathway inhibition resulted in NF ‐ κ B inactivation and down‐regulation of i NOS and COX ‐2 protein expression. Taken together, baicalin treatment effectively protected keratinocytes from UVB ‐induced inflammatory damage through TLR pathway modulation.