Promotion Effect of Apo-9'-fucoxanthinone from Sargassum muticum on Hair Growth via the Activation of Wnt/ß-Catenin and VEGF-R2.

This study was conducted to evaluate the effects of Sargassum muticum extract and apo-9'-fucoxanthinone, a principal component of S. muticum, on hair growth. When rat vibrissa follicles were treated with S. muticum extract for 21 d, the hair-fiber lengths for the vibrissa follicles increased significantly. Treatment with the S. muticum extract and the EtOAc fraction of the S. muticum extract markedly increased the proliferation of dermal papilla cells (DPCs) and decreased the 5α-reductase activity. In addition, the EtOAc fraction of the S. muticum extract significantly promoted anagen initiation in C57BL/6 mice. Especially, apo-9'-fucoxanthinone, an active constituent from the S. muticum extract, caused an increase in DPC proliferation and a decrease in 5α-reductase activity. To elucidate the molecular mechanisms of apo-9'-fucoxanthinone on the proliferation of DPCs, we examined the level of various signaling proteins. Apo-9'-fucoxanthinone increased the level of vascular endothelial growth factor receptor-2 (VEGF-R2), Wnt/ß-catenin signaling proteins such as phospho(ser9)-glycogen synthase kinase-3ß (GSK-3ß) and phospho(ser552)-ß-catenin, whereas apo-9'-fucoxanthinone did not affect the transforming growth factor-ß (TGF-ß) signaling proteins such as Smad2/3. These results suggest that apo-9'-fucoxanthinone from S. muticum could have the potential for hair growth with DPC proliferation via the activation of Wnt/ß-catenin signaling and the VEGF-R2 pathway.

Photo-protective effect of sargachromenol against UVB radiation-induced damage through modulating cellular antioxidant systems and apoptosis in human keratinocytes.

The aim of this study was to evaluate the photo-preventive effects of sargachromenol (SC) against ultraviolet B (UVB)-induced oxidative stress in human keratinocytes via assessing the antioxidant properties and underlying molecular mechanisms. SC exhibited a significant scavenging effect on UVB-induced intracellular reactive oxygen species (ROS). SC attenuated UVB-induced oxidative macromolecular damage, including the protein carbonyl content, DNA strand break, and 8-isoprostane level. Furthermore, SC decreased UVB-induced Bax, cleaved caspase-9, and cleaved caspase-3 protein levels, but increased that of Bcl-2, which are well-known key mediators of apoptosis. Moreover, SC increased superoxide dismutase, catalase, and heme oxygenase-1 protein expression. Pre-treatment with SC upregulated the main transcription factor of antioxidant enzymes, erythroid 2-related factor 2 level, which was reduced by UVB irradiation. Extracellular signal-regulated kinase (ERK) and Jun N-terminal kinases (JNK) are involved in the regulation of many cellular events, including apoptosis. SC treatment reversed ERK and JNK activation induced by UVB. Collectively, these data indicate that SC can provide remarkable cytoprotection against the adverse effects of UVB radiation by modulating cellular antioxidant systems, and suggest the potential of developing a medical agent for ROS-induced skin diseases.