This study was conducted to identify the anti-melanogenesis constituents from a seaweed Dictyota coriacea (Holmes). Three known compounds, viz. 1,9-dihydroxycrenulide (1), epiloliolide (2) and D-mannitol (3), were isolated from the ethanol extract. The melanin synthesis inhibition activities were evaluated using B16F10 melanoma cells for the isolates. Compared with the positive control, arbutin, compounds 1 and 2 exhibited more potency, showing 27.8 and 22.6 % inhibition activities at a substrate concentration of 30 μg/mL. Our studies also indicate that these compounds are not cytotoxic. Hence, they might prove to be useful therapeutic agents for treating hyperpigmentation and effective components of whitening cosmetics.

Several compounds and extracts isolated from a brown alga, Ishige (I.) okamurae, exhibit anti-oxidant and anti-inflammatory effects. The present study investigated whether the ethyl acetate (EtOAc) fraction of I. okamurae (EFIO) could ameliorate carbon tetrachloride (CCl 4)-induced hepatotoxicity in rats. Sprague-Dawley rats were intraperitoneally (i.p.) administered with EFIO at 10 or 50 mg/kg per day for 2 consecutive days before CCl 4 injection (3.3 mL/kg, i.p.). Twenty four hours later, the rats were anesthesized with diethyl ether and dissected. Pretreatment with EFIO significantly reduced the increased serum levels of alanine aminotransferase and aspartate aminotransferase in CCl 4 -treated rats. Pretreatment with EFIO also significantly inhibited the reduced activities of superoxide dismutase and catalase in the CCl 4 -injured liver. Histopathological evaluations showed that hemorrhage, hepatocyte necrosis, inflammatory cell infiltration, and fatty degeneration induced by CCl 4 treatment were ameliorated by the administration of EFIO. Additionally, liver immunohistochemical analyses revealed the marked reduction in ED1-positive monocyte-like macrophages in EFIO-pretreated rats given CCl 4 . These results suggest that EFIO ameliorates CCl 4 -induced liver injury, possibly through the inhibition of oxidative stress.