The bioimaging of acute effects on the cutaneous microcirculation by UVB exposure

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OBJECTIVE: We previously demonstrated that ultraviolet B (UVB: wave length 280 . 315 nm) irradiation to mouse skin induced acute microcirculatory effects, i.e., vascular dilation, increase in vascular permeability and leukocyte-endothelial interaction, which was caused by reactive oxygen due to UVB. The objective of the present study was to evaluate effects of anti-oxidants such as vitamin E (VE) and green tea catechins (GTC) on leukocyte-endothelial interactions by UVB irradiation (UVBIR) using the mouse-dorsal skin chamber (DSC) as an experimental model.METHODS: DSCs were installed to female hairless HR-1 mice by surgical procedure at least 72 hours prior to the experiment. We examined 4 experimental conditions; UVBIR only, anti P-selectin antibody treatment+UVBIR, VE administration+UVBIR and GTC administration+UVBIR. To visualize the leukocytes behaviors in vivo, a bolus of rhodamine 6G solution was injected into tail vein prior observation. Before and after UVBIR (240 mJ/cm2) to th … More e skin within the chamber, fluorescent images at the same microvasculature were recorded by using a fluorescence microscopy under conscious conditions. Off-line analysis of the leukocyte-endothelial interaction was done by counting numbers adhering and rolling leukocytes within venules for 30 sec per unit area. VE was administrated twice a day (25 μl/each) for 3 days and 1 hour before the UVBIR via feeding tube. Dissolved GTC in water (10mg/each) was administrated 1 hour before the UVBIR via feeding tube. RESULTS: The mean value of rolling leukocytes number was significantly higher in the venules at 6 hours after UVBIR than that in pre-UVBIR. This increase was suppressed when anti-mouse P-selectin antibody was injected into tail vein prior to UVBIR. When VE or GTC was administrated prior to UVBIR, increase of rolling leukocytes number was also suppressed.CONCLUSIONS: Our findings suggest that the administrations of anti-oxidants show the preventive effect on UVB induced leukocyte-endothelial interaction which is mainly mediated by P-selectin. Less