An immunomodulatory polysaccharide (DAP4) was extracted, purified, and characterized from Durvillaea antarctica. The results of chemical and spectroscopic analyses demonstrated that the polysaccharide was a fucoidan, and was mainly composed of (1→3)-α-l-Fucp and (1→4)-α-l-Fucp residues with a small degree of branching at C-3 of (1→4)-α-l-Fucp residues. Sulfate groups were at C-4 of (1→3)-α-l-Fucp, C-2 of (1→4)-α-l-Fucp and minor C-6 of (1→4)-β-d-Galp. Small amounts of xylose and galactose exist in the forms of β-d-Xylp-(1→ and β-d-Gal-(1→. The immunomodulatory activity of DAP4 was measured on RAW 264.7 cells, the results proved that DAP4 exhibited excellent immunomodulatory activities, such as promoted the proliferation of spleen lymphocytes, increased NO production, as well as enhanced phagocytic of macrophages. Besides, DAP4 could also produce better enhancement on the vitality of NK cells. For the high immunomodulatory activity, DAP4 might be a potential source of immunomodulatory fucoidan with a novel structure.

κ-Selenocarrageenan (KSC) is an organic selenium (Se) polysaccharide. There has been no report of an enzyme that can degrade κ-selenocarrageenan to κ-selenocarrageenan oligosaccharides (KSCOs). This study explored an enzyme, κ-selenocarrageenase (SeCar), from deep-sea bacteria and produced heterologously in Escherichia coli, which degraded KSC to KSCOs. Chemical and spectroscopic analyses demonstrated that purified KSCOs in hydrolysates were composed mainly of selenium-galactobiose. Organic selenium foods through dietary supplementation could help regulate inflammatory bowel diseases (IBD). This study discussed the effects of KSCOs on dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in C57BL/6 mice. The results showed that KSCOs alleviated the symptoms of UC and suppressed colonic inflammation by reducing the activity of myeloperoxidase (MPO) and regulating the unbalanced secretion of inflammatory cytokines (tumor necrosis factor (TNF)-α, interleukin (IL)-6 and IL-10). Furthermore, KSCOs treatment regulated the composition of gut microbiota, enriched the genera Bifidobacterium, Lachnospiraceae_NK4A136_group and Ruminococcus and inhibited Dubosiella, Turicibacter and Romboutsia. These findings proved that KSCOs obtained by enzymatic degradation could be utilized to prevent or treat UC.

Although it is well recognized that mycosporine-like amino acids (MAAs) are ultraviolet (UV) protective agents that can reduce UV damage, the specific biological mechanism of its role in the skin remains unclear. In this study, we investigated the effect of MAAs extracted from Antarctic diatom Phaeodactylum tricornutum ICE-H on UVB-induced skin damage using a mice model. The MAAs components identified by liquid chromatography-tandem mass spectrometry included 4-deoxygadusol, shinorine, and porphyra-334, which were purified using a Supledean Carboxen1000 solid phase extraction column. The antioxidant activities of these MAA compounds were tested in vitro. For UVB-induced skin photodamage in mice, MAAs alleviated skin swelling and epidermal thickening in this study. We detected the content of reactive oxygen species (ROS), malondialdehyde, and collagen in skin tissue. In addition, quantitative real-time polymerase chain reaction was used to detect nuclear factor-κB (NF-κB), tumor necrosis factor α, interleukin-1β, cyclooxygenase-2, mitogen activated protein kinase (MAPK) family (extracellular signal-regulated kinase, c-Jun amino-terminal kinase, and p38 kinase), and matrix metalloproteinases. The expression of these cytokines and enzymes is related to inflammatory responses and collagen degradation. In comparison to the model group without MAA treatment, the MAA component decreased the concentration of ROS, the degree of oxidative stress in the skin tissue, and the expression of genes involved in the NF-κB and MAPK pathways. In summary, these MAA components extracted from Phaeodactylum tricornutum ICE-H protected against UVB-induced skin damage by inhibiting ROS generation, relieving skin inflammation, and slowing down collagen degradation, suggesting that these MAA components are effective cosmetic candidate molecules for the protection and therapy of UVB damage.

The previous study successfully established an expression strain of ζ-carotene-like compounds (CLC) and demonstrated its remarkable antioxidant activity, which exhibited resistance to photodamage caused by UVB radiation on the skin following gavage administration. The objective of this study was to investigate the impact and mechanism of CLC on UVB-induced skin damage through topical application. Cell viability, anti-apoptotic activity, ROS scavenging ability, the inhibition of melanin synthesis, the regulation of inflammatory factors and collagen deposition were assessed in cells and mice using qRT-PCR, WB, Elisa assays, immunohistochemistry staining and biochemical kits, etc. The experimental results demonstrated that CLC-mitigated apoptosis induced by UVB irradiation up-regulated the Keap1/Nrf2/ARE antioxidant pathway to attenuate levels of ROS and inflammatory factors (NF-κB, TNF-α, IL-6 and IL-β), and suppressed MAPK/AP-1 and CAMP/PKA/CREB signaling pathways to mitigate collagen degradation, skin aging and melanin formation. In conclusion, this study underscored the potential of CLC as a safe and efficacious source of antioxidants, positioning it as a promising ingredient in the formulation of cosmetics targeting anti-aging, skin brightening and sunburn repair.

Mycosporine-glycine (M-Gly), a member of the mycosporine-like amino acid (MAA) family, is known for its potent antioxidant and anti-inflammatory properties. However, its in vivo efficacy in alleviating acute skin photodamage, primarily caused by oxidative stress, has not been well explored. In this investigation, 30 female ICR mice were divided into four groups: a control group and three Ultraviolet B (UVB)-exposed groups treated with saline or M-Gly via intraperitoneal injection for 30 days. At the end of the experiment, UVB exposure caused erythema, wrinkling, collagen degradation, and mast cell infiltration in mouse dorsal skin. M-Gly treatment improved skin appearance and reduced mast cell numbers, while also elevating antioxidant levels, including superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH). Furthermore, M-Gly reduced inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and IL-1β, typically upregulated after UVB exposure. M-Gly also protected skin collagen by upregulating type I procollagen and decreasing MMP-1 levels. Skin metabolomic profiling identified 34 differentially abundant metabolites, and transcriptomic analysis revealed 752 differentially expressed genes. The combined metabolomic and transcriptomic data indicate that M-Gly’s protective effects may involve the regulation of ion transport, cellular repair, metabolic stability, collagen preservation, and the Nrf2/HO-1 pathway. These findings highlight M-Gly’s potential as an endogenous antioxidant for protecting skin from UVB-induced damage.

Polysaccharides derived from green algae have garnered significant attention owing to their distinctive structural characteristics and biological activities. In particular, sulfated polysaccharides from these algae represent a promising frontier in the discovery of novel therapeutic agents. In this present study, a sulfated galactan from Caulerpa taxifolia, designated SGC, was obtained by dilute alkali extraction and chromatographic purification. On the basis of chemical and spectroscopic analyses, the backbone of SGC was constituted by a backbone of →3)-β-d-Galp-(1→ with sulfate substitution at the C-2 and a branch on C-6. The side chains contained →6)-β-d-Galp(2SO₄)-(1→, →6)-β-d-Galp(3OMe)-(1→ and →3)-β-d-Galp(4,6-Pyr)-(1→ units. SGC possessed strong hypoglycemic activity in vitro, as evaluated by an assay of α-amylase inhibition. The anti-diabetic activity of SGC in vivo was further investigated using T2DM mice induced by high-fat diet combined with streptozotocin. The results indicated that SGC markedly restored body weight, reduced fasting blood glucose and possessed a significant glucose-regulating effect. Furthermore, SGC effectively increased insulin sensitivity and mitigated insulin resistance. Additionally, SGC effectively regulated lipid metabolism and alleviated oxidative stress. Notably, SGC ameliorated liver and pancreas damage induced by high-fat diet combined with streptozotocin. The investigation demonstrates that SGC is a unique sulfated galactan and has potential as a novel anti-diabetic agent.