Article date: October 2002
By: Soo Mi Ahn, Hyoung‐Young Yoon, Byung Gon Lee, Kyoung Chan Park, Jin Ho Chung, Chang‐Hyun Moon, Soo Hwan Lee in Volume 137, Issue 4, pages 497-503
Fructose‐1,6‐diphosphate (FDP), a glycolytic metabolite, is reported to ameliorate inflammation and inhibit the nitric oxide production in murine macrophages stimulated with endotoxin. It is also reported that FDP has cytoprotective effects against hypoxia or ischaemia/reperfusion injury in brain and heart. However, underlying mechanisms of its various biological activities are not completely understood.
In this study, we examined the effects of FDP on UVB‐induced prostaglandin production in HaCaT keratinocytes.
Ultraviolet B (UVB, 280–320 nm) irradiation (30 mJ cm−2) increased prostaglandin E2(PGE2) production, which was significantly decreased by FDP in a concentration dependent manner. NS‐398, a cyclo‐oxygenase‐2 (COX‐2) selective inhibitor completely inhibited UVB‐induced PGE2 production showing that COX‐2 activity is responsible for the increase in PGE2 production under our experimental conditions.
UVB irradiation increased total COX activity and COX‐2 mRNA in HaCaT keratinocytes, which were significantly blocked by FDP in a concentration dependent manner.
N‐acetylcysteine (NAC) significantly attenuated UVB‐induced PGE2 production, COX activity and COX‐2 mRNA expression indicating oxidative components might contribute to these events.
FDP reduced UVB‐induced increase in cellular reactive oxygen species (ROS) level although it did not show direct radical scavenging effect in the experiment using 1,1‐diphenyl‐2picrylhydrazil (DPPH). FDP preserved the cellular antioxidant capacity including catalase activity and GSH content after irradiation.
Our data obtained hitherto suggest that FDP may have a protective role in UVB‐injured keratinocyte by attenuating PGE2 production and COX‐2 expression, which are possibly through blocking intracellular ROS accumulation.
Fructose‐1,6‐diphosphate (FDP), a glycolytic metabolite, is reported to ameliorate inflammation and inhibit the nitric oxide production in murine macrophages stimulated with endotoxin. It is also reported that FDP has cytoprotective effects against hypoxia or ischaemia/reperfusion injury in brain and heart. However, underlying mechanisms of its various biological activities are not completely understood.
In this study, we examined the effects of FDP on UVB‐induced prostaglandin production in HaCaT keratinocytes.
Ultraviolet B (UVB, 280–320 nm) irradiation (30 mJ cm−2) increased prostaglandin E2(PGE2) production, which was significantly decreased by FDP in a concentration dependent manner. NS‐398, a cyclo‐oxygenase‐2 (COX‐2) selective inhibitor completely inhibited UVB‐induced PGE2 production showing that COX‐2 activity is responsible for the increase in PGE2 production under our experimental conditions.
UVB irradiation increased total COX activity and COX‐2 mRNA in HaCaT keratinocytes, which were significantly blocked by FDP in a concentration dependent manner.
N‐acetylcysteine (NAC) significantly attenuated UVB‐induced PGE2 production, COX activity and COX‐2 mRNA expression indicating oxidative components might contribute to these events.
FDP reduced UVB‐induced increase in cellular reactive oxygen species (ROS) level although it did not show direct radical scavenging effect in the experiment using 1,1‐diphenyl‐2picrylhydrazil (DPPH). FDP preserved the cellular antioxidant capacity including catalase activity and GSH content after irradiation.
Our data obtained hitherto suggest that FDP may have a protective role in UVB‐injured keratinocyte by attenuating PGE2 production and COX‐2 expression, which are possibly through blocking intracellular ROS accumulation.
British Journal of Pharmacology (2002) 137, 497–503. doi:10.1038/sj.bjp.0704896
DOI: 10.1038/sj.bjp.0704896
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