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Topical application of Nexrutine inhibits ultraviolet B‐induced cutaneous inflammatory responses in SKH ‐1 hairless mouse
Author(s) -
Alam Shamshad,
Pal Anu,
Singh Dhirendra,
Ansari Kausar Mahmood
Publication year - 2018
Publication title -
photodermatology, photoimmunology and photomedicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.736
H-Index - 60
eISSN - 1600-0781
pISSN - 0905-4383
DOI - 10.1111/phpp.12348
Subject(s) - hairless , inflammation , chemistry , sunburn , western blot , nitric oxide synthase , myeloperoxidase , proinflammatory cytokine , croton oil , pharmacology , immunology , microbiology and biotechnology , nitric oxide , medicine , biology , biochemistry , dermatology , organic chemistry , gene
Summary Background Ultraviolet B ( UVB ) radiation is the major contributor to skin inflammation which leads to the development of skin cancer. Hence, in this study, we studied the effect of Nexrutine ( NX ) on UVB ‐induced cutaneous inflammation and its mediators. Methods Ultraviolet absorption spectra of NX were measured by spectrophotometer. To conduct the photoprotective studies, SKH ‐1 hairless mice were topically treated with NX , 30 minutes before to the UVB (180 mJ/cm 2 ) exposure. Twenty hours of post‐ UVB irradiation, mouse skin was used for edema measurements, H & E staining, myeloperoxidase ( MPO ) activity, and estimation of plasma cytokines. In addition, expression levels of inflammatory cytokines, cyclooxygenase‐2 ( COX ‐2), and inducible nitric oxide synthase ( iNOS ) were also determined by Western blot analysis. Results Nexrutine displayed absorbance over the UVB spectrum. NX significantly decreased the UVB ‐induced epidermal edema, skin thickness, leukocyte infiltration, number of the sunburn, and TUNEL ‐positive cells. NX treatment also decreased the number of mast cells, MPO activity, expression of pro‐inflammatory cytokines, and inflammation mediator protein in mouse skin. Conclusion These results provide evidences that NX inhibits the UVB ‐induced cutaneous inflammatory responses in SKH ‐1 mouse skin.