1 Fructose-1,6-diphosphate (FDP), a glycolytic metabolite, is reported to ameliorate in¯ammation and inhibit the nitric oxide production in murine macrophages stimulated with endotoxin. It is also reported that FDP has cytoprotective eects against hypoxia or ischaemia/reperfusion injury in brain and heart. However, underlying mechanisms of its various biological activities are not completely understood. 2 In this study, we examined the eects of FDP on UVB-induced prostaglandin production in HaCaT keratinocytes. 3 Ultraviolet B (UVB, 280 ± 320 nm) irradiation (30 mJ cm 72 ) increased prostaglandin E 2 (PGE 2 ) production, which was signi®cantly decreased by FDP in a concentration dependent manner. NS-398, a cyclo-oxygenase-2 (COX-2) selective inhibitor completely inhibited UVB-induced PGE 2 production showing that COX-2 activity is responsible for the increase in PGE 2 production under our experimental conditions. 4 UVB irradiation increased total COX activity and COX-2 mRNA in HaCaT keratinocytes, which were signi®cantly blocked by FDP in a concentration dependent manner. 5 N-acetylcysteine (NAC) signi®cantly attenuated UVB-induced PGE 2 production, COX activity and COX-2 mRNA expression indicating oxidative components might contribute to these events. 6 FDP reduced UVB-induced increase in cellular reactive oxygen species (ROS) level although it did not show direct radical scavenging eect in the experiment using 1,1-diphenyl-2picrylhydrazil (DPPH). FDP preserved the cellular antioxidant capacity including catalase activity and GSH content after irradiation. 7 Our data obtained hitherto suggest that FDP may have a protective role in UVB-injured keratinocyte by attenuating PGE 2 production and COX-2 expression, which are possibly through blocking intracellular ROS accumulation.