2010 Volume 48 Issue 1 Pages 42-49
PURPOSE: It is commonly accepted that sunburn is usually occurred within a couple of hours after Ultraviolet B (UVB) irradiation. However, we recently demonstrated that increased microvascular permeability and vasodilatation of venules were observed within a few minutes after UVB irradiation to the skin in mice. To elucidate mechanisms to be involved, we used various pharmacological inhibitors concurrently with UVB irradiation. METHODS: Dorsal Skinfold Chamber (DSC) and fluorescence intravital-microscopy techniques were applied to Hos: HR-1 hairless mice for measuring the microcirculatory parameters including vascular permeability, vascular diameter, and leukocyte behavior by using fluorescent dye. L-NAME (NOS inhibitor) . Edaravone (free radical scavenger) . Indomethacin (non-selective COX inhibitor) . and Celecoxib (COX-2 selective inhibitor) were administrated to the mice prior to UVB irradiation and evaluated the efficacy of each inhibitor on microvascular events mentioned above. RESULTS&CONCLUSION: A significant increase in vascular permeability, venular diameter and rolling and/sticking leukocyte counts was observed within a few minutes after UVB irradiation at 240mJ/cm2. The increased vascular permeability was significantly reduced by administration of all the inhibitors. In contrast, increase in venular diameter and rolling/sticking leukocyte counts was not affected. These results indicate that the increase of vascular permeability within a few minutes after UVB irradiation is related to ROS, NOS and COX activation. The reaction of vascular permeability is a common signal pathway at the inflammation process including sunburn. These results suggest that the common signal pathway under inflammation process may be also involved immediately after UVB irradiation.
