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.
Liang et al. (Wed,) studied this question.