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Edible Brown Seaweed Sargassum fusiforme (Harvey) Setchell, 1931 abbreviated as Sargassum fusiforme was used for folk medical therapy in East Asia countries over five hundred years. Saringosterol acetate (SA) was isolated from S. fusiforme in our previous study and indicated various effects. However, anti-obesity activity of SA and its mechanism still unknown.The inhibitory effect of SA, isolated from S. fusiforme, on adipogenesis in 3T3-L1 adipocytes was investigated in vitro and in zebrafish model. Cell toxicity, differentiation, signaling pathway, and lipid accumulation of SA treated 3T3-L1 adipocytes were determined. The body weight and triglyceride content of diet-induced obese (DIO) adult male zebrafish were measured from 12 to 17 weeks after fertilization.SA attenuated the differentiation of cells and reduced lipid accumulation, and triglyceride content in the 3T3-L1 adipocytes. During the differentiation of adipocytes, SA suppressed fat accumulation and decreased the expression of signal factors responsible for adipogenesis. In SA-treated adipocytes, while fatty acid synthetase was downregulated, AMP-activated protein kinase (AMPK) was upregulated. Furthermore, SA suppressed body weight and triglyceride content in DIO zebrafish.SA is a potential therapeutic agent in the management of metabolic disorders, such as obesity.

Sargassum fusiformis is among the most important edible brown seaweeds in Eastern Asia that contains various bioactive compounds and strong activities. Saringosterol acetate (SA) was successfully isolated from S. fusiformis in our previous research. In this study, SA was investigated for its anticancer effect on MCF-7 breast cancer cells. SA attenuated the survival rate of MCF-7 cells with an IC

We had observed in our previous study that the active fucoidan (JHCF4), isolated from the crude fucoidan in acid-processed Hizikia fusiforme, possessed an anticancer effect. In this study, the antioxidant effect of JHCF4 was evaluated. Among the fractions, JHCF4 showed the highest scavenging activity against 2, 2-diphenyl-1-picrylhydrazyl (DPPH), alkyl, and hydroxyl radicals, as well as protective effect against reactive oxygen species (ROS) in 2, 2'-azobis (2-amidinopropane) dihydrochloride (AAPH)-treated Vero cells. Furthermore, JHCF4 showed a protective activity against AAPH-induced apoptosis, as observed by nuclear staining with Hoechst 33342. Our results showed that JHCF4 can up-regulate Bcl-xL, down-regulate Bax and cleave caspase-3 with increased concentrations in AAPH-induced Vero cells. JHCF4 induced anti-apoptosis via a mitochondria-mediated pathway. Additionally, JHCF4 was selected for further in vivo screening in a zebrafish model, which markedly decreased ROS generation and lipid peroxidation. Thus, JHCF4 showed a potential protective activity against AAPH-induced ROS both in vitro and in the zebrafish model.

The aim of this study was to investigate the antiproliferative effects of fucoidan from three regional hijiki (Hizikia fusiforme) samples (Zhejiang-China, Jeju-Korea [JH], and Wando-Korea) in East Asia. Hijiki was processed using 1% citric acid to decrease heavy metal content. The JH sample was separated using diethylaminoethyl-cellulose-ion exchange chromatography to obtain four active fractions (JHCF1-JHCF4) and their monosaccharide composition was detected using high-performance liquid chromatography. The structure of the crude polysaccharides and four fucoidan fractions was analyzed using Fourier-transform infrared spectroscopy. JHCF4 showed the highest fucose and sulfate content and decreased Hep3B cell growth in 48 h with a half-maximal inhibitory concentration of 33.53 ± 2.50 μg/ml, which represented the strongest anticancer activity. Further, nuclear staining with Hoechst 33342 and acridine orange-ethidium bromide staining demonstrated that the anticancer activity of JHCF4 was mediated by apoptosis. Moreover, JHCF4 down-regulated B-cell lymphoma extra-large, while up-regulating Bcl-2-associated X protein, caspase-3, and apoptotic bodies to different degrees in Hep3B cells. JHCF4 induced apoptosis via the generation of reactive oxygen species along with the concurrent loss of mitochondrial membrane potential, indicating the potential role of the mitochondria-mediated pathway. Therefore, these results indicate that JHCF4 exhibited antiproliferative effects on the investigated cancer cell lines.