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Fructose-1,6-diphosphate attenuates prostaglandin E2 production and cyclo-oxygenase-2 expression in UVB-irradiated HaCaT keratinocytes.
| Content Provider | Semantic Scholar |
|---|---|
| Author | Ahn, Soo Mi Yoon, Hana Lee, Byung Gon Park, Kyoung-Chan Chung, Jin Ho Moon, C. H. Lee, Jong Kwon |
| Copyright Year | 2002 |
| Abstract | 1. 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. 2. In this study, we examined the effects of FDP on UVB-induced prostaglandin production in HaCaT keratinocytes. 3. Ultraviolet B (UVB, 280-320 nm) irradiation (30 mJ cm(-2)) increased prostaglandin E(2)(PGE(2)) 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 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 significantly blocked by FDP in a concentration dependent manner. 5. N-acetylcysteine (NAC) significantly 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 effect 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. |
| Starting Page | 497 |
| Ending Page | 503 |
| Page Count | 7 |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | http://repository.ajou.ac.kr/bitstream/201003/3414/3/497-503.pdf |
| PubMed reference number | 12359631v1 |
| Volume Number | 137 |
| Issue Number | 4 |
| Journal | British journal of pharmacology |
| Language | English |
| Access Restriction | Open |
| Subject Keyword | Acetylcysteine Alprostadil Biologic Preservation CATALASE Cyclooxygenase Inhibitors Dinoprostone Endotoxins Glutathione Hypoxia Ischemia NS 398 Nitric Oxide Prostaglandin E2 Prostaglandin Production Prostaglandin-Endoperoxide Synthase Prostaglandins Reactive Oxygen Species Reperfusion Injury Reperfusion Therapy Ultraviolet B radiation fructose-1,6-diphosphate keratinocyte |
| Content Type | Text |
| Resource Type | Article |
