It is well known that ultraviolet B irradiation leads to dermal
inflammation. In this study, we found that
Mekabu fucoidan suppressed
edema, decreased the thickness of the prickle cell layer, and decreased
matrix metalloproteinase 1 in the skin of mice irradiated with ultraviolet B. Moreover, we found that the mean level of
interferon gamma of
Mekabu fucoidan-treated, ultraviolet B-irradiated mice (approximately 2.2 ng/mL) was not significantly different from that in normal mice (approximately 2.5 ng/mL). In contrast, a significant decrease in the mean level of
interferon gamma (approximately 1.3 ng/mL) in ultraviolet B-irradiated control mice was observed compared with that in
Mekabu fucoidan-treated, ultraviolet B-irradiated mice. The mean thickness of the prickle cell layer in the skin of
Mekabu fucoidan-treated, ultraviolet B-irradiated mice was less than that in the ultraviolet B-irradiated control mice.
Metalloproteinase 1 activity was significantly higher in the skin of ultraviolet B-irradiated mice than in the skin of untreated, nonirradiated normal mice.
Metalloproteinase 1 in the skin of ultraviolet B-irradiated,
Mekabu fucoidan- or
L(+)-ascorbic acid (
vitamin C)-treated mice was significantly lower than that in the ultraviolet B-irradiated control mice. Mitigation of the morphological changes in
Mekabu fucoidan-treated mice was correlated with a decrease in
metalloproteinase 1 levels. These data indicate that
Mekabu fucoidan is an effective suppressor of
inflammation in an ultraviolet B-irradiated mouse model.