表皮角化細胞におけるNO産生およびNOS発現への中波長紫外線照射の効果

抄録

UV radiation causes inflammation characterized by erythema and swelling, immunosuppression, apoptosis, melanogenesis, photoaging, and photocarcinogenesis, whereas it also exhibits anti-inflammatory or therapeutic effects as seen in the treatment of psoriasis and atopic dermatitis. Nitric oxide (NO), a reactive gaseous molecule with multiple cellular functions, has been speculated to play pathogenic or protective roles in inflammatory dermatoses. Therefore, it is important to elucidate how UVB radiation regulates or modifies NO production and nitric oxide synthase (NOS) expression in skin. To examine this issue, we used murine cultured keratinocyte Pam 212 cells and found that low doses of UVB radiation significantly suppressed NO production and inducible NOS (iNOS) expression in keratinocytes stimulated by IFN-γ or TNF-α. Taking pathogenic roles of excessive NO produced through iNOS induction into consideration, UVB-induced suppression of NO production may explain in part the anti-inflammatory or therapeutic effects of UVB radiation in inflammatory dermatoses. However, in keratinocytes under nonstimulated condition, UVB radiation increased NO production, where brain NOS (bNOS) mRNA and protein expressions were enhanced and iNOS mRNA expression was suppressed. These results suggest that NO thus produced after UVB radiation in non-inflammatory skin may explain in part the subsequent erythema formation, melanogenesis and other UVB-induced skin reactions.