Topical application of Nexrutine inhibits ultraviolet B-induced cutaneous inflammatory responses in SKH-1 hairless mouse.

Abstract

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. Ultraviolet absorption spectra of NX were measured by spectrophotometer. To conduct the photoprotective studies, SKH-1 hairless mice were topically treated with NX, 30minutes before to the UVB (180mJ/cm2 ) 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. 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. These results provide evidences that NX inhibits the UVB-induced cutaneous inflammatory responses in SKH-1 mouse skin.