Ultraviolet B (UVB) radiation is a major contributing factor to skin photoaging by accelerating inflammation and collagen degradation. This underscores the critical need to develop natural and safe bioactive compounds to combat UVB-induced skin disease. In this study, different chitosan Maillard reaction products (CMRPs) were prepared and characterized to evaluate their anti-photoaging activities, mechanisms of action and safety. The Maillard reaction altered the morphology of chitosan from a loose powder into a crosslinked structure. The resulting CMRPs exhibited enhanced DPPH and ABTS radical scavenging activities as well as increased elastase inhibitory effects. All six CMRPs were non-toxic to HaCaT cells and improved the viability of UVB-induced photoaged cells, with CG-6 demonstrating the most potent anti-photoaging activity. Mechanistic investigations revealed that CG-6 significantly inhibited the accumulation of reactive oxygen species (ROS) in photoaged HaCaT cells, enhanced the activities of antioxidant enzymes such as superoxide dismutase (SOD) and catalase (CAT), suppressed the expression of matrix metalloproteinases (MMPs) and inflammatory factors, and regulated the expression of key genes in the MAPK signaling pathway, thereby exerting protective effects against photoaging. Oral administration of CG-6 for 28 days did not cause any apparent organ damage in mice. There were no significant differences in organ indices, histopathological examination, hematological parameters, liver and kidney function markers, or antioxidant enzyme activity levels between the CG-6-treated and control groups. These findings indicate that CG-6 does not cause negative effect on the health of mice. Overall, this study provides a strong theoretical foundation for the application of Maillard reaction products, particularly CG-6 in the development of anti-photoaging functional foods.

Excessive ultraviolet B (UVB) exposure disrupt the skin barrier, provoking inflammation. This study investigated the protective effects of a degraded Sargassum fusiforme polysaccharide (DSFP-45) against UVB-induced barrier dysfunction in HaCaT keratinocytes and BALB/c nude mice. DSFP-45 significantly improved cell viability, reduced reactive oxygen species, and restored barrier-protiens (filaggrin, loricrin, and aquaporin 3) in UVB-irradiated HaCaT cells. It suppressed pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6) by inhibiting the PI3K/Akt/NF-κB pathway. In vivo, oral and topical DSFP-45 alleviated erythema, reduced transepidermal water loss, preserved collagen and elastic fibers, normalized ceramide levels, and suppressed pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6). The 16s rRNA sequencing showed that DSFP-45 increased beneficial skin microbiota (Staphylococcus and Lactobacillus), and reduced harmful taxa (Corynebacterium, Streptococcus, and Stenotrophomonas). Kyoto Encyclopedia of Genes and Genomes (KEGG) metabolic pathway analysis showed that the skin microbiota under DSFP-45 treatment influence biosynthesis of amino acids and biosynthesis of secondary metabolites. These findings demonstrate that DSFP-45 protected against UVB-induced skin barrier damage by enhancing barrier protein expression, dampening inflammation, and possibly by modulating skin microbiota, supporting its potential as a natural anti-photodamage agent.

Osteoporosis, a prevalent skeletal disorder aggravated by estrogen deficiency, is a major global health concern that presents significant clinical challenges, particularly for postmenopausal women. This study evaluates the therapeutic potential of colostrum whey protein (CWP) in mitigating estrogen deficiency-induced osteoporosis through both in vivo (ovariectomized murine model) and in vitro (osteoblast culture) approaches. In ovariectomized (OVX) mice, CWP administration increased bone mineral density (BMD) by 45%, elevated trabecular number (Tb.N) by 38%, restored trabecular thickness (Tb.Th), and reduced trabecular separation (Tb.Sp) by 40%. Histomorphometric analysis confirmed enhanced trabecular structure, collagen restoration, and reduced osteoclast activity. CWP also restored bone metabolism by increasing alkaline phosphatase (ALP) and osteoprotegerin (OPG) levels, while decreasing receptor activator of nuclear factor kappa-B ligand (RANKL) and tartrate-resistant acid phosphatase (TRAP) levels. Mechanistic studies showed that CWP modulated the hepatic-bone axis through suppression of PP2ACα and induction of lecithin-cholesterol acyltransferase (LCAT), facilitating cholesterol transport. Furthermore, CWP upregulated osteogenic markers (bone morphogenetic protein-2 (BMP-2), runt-related transcription factor-2 (RUNX-2), and activated MAPK, BMP/Smad, and WNT/β-catenin signaling pathways, promoting osteoblast proliferation, differentiation, and mineralization in vitro. These findings highlight CWP’s dual role in enhancing bone formation and inhibiting resorption through both local (osteoblast activation) and systemic (hepatic-bone axis modulation) mechanisms. Collectively, CWP emerges as a promising multi-target therapeutic candidate for osteoporosis, bridging bone remodeling and metabolic crosstalk. Additional translational studies are warranted to validate its clinical efficacy.

High molecular weights of seaweed polysaccharides usually limit their bioavailability. Fermentation of polysaccharides can reduce their molecular weight and improve their bioactivity, which effectively increase their application in food industry. In this study, Lactobacillus plantarum was used to ferment Sargassum fusiforme polysaccharides (SFP). The structure of fermented polysaccharide was characterized. Results showed that fermentation drastically reduced the average molecular weight of SFP by 75.2%. The percentage of reducing sugars and uronic acid gradually increased with time during fermentation. The functional groups of the fermented polysaccharides did not change, but the apparent morphology changed from rough and porous to smooth and fragmented. Fermented SFP exhibited better anti-photoaging activity in UVB-irradiated HaCaT cells. Specifically, it increased cell viability and hydroxyproline level. Additionally, it promoted the gene expression of Pro-collagen I α1 synthesis while inhibiting matrix metalloproteinases (MMP-1, MMP-3, MMP-9) and pro-inflammatory cytokines (IL-1β, TNF-α). These findings suggested that fermentation could enhance the anti-photoaging activity of seaweed polysaccharide, and could be developed as an alternative method for degrading polysaccharides.