Fucoidan from Saccharina japonica Alleviates Hyperuricemia-Induced Renal Fibrosis through Inhibiting the JAK2/STAT3 Signaling Pathway

Fucoidan is a native sulfated polysaccharidemainly isolated frombrown seaweed, with diverse pharmacological activities, such as anti-inflammatoryand antifibrosis. Hyperuricemia (HUA) is a common metabolic diseaseworldwide and mainly causes hyperuricemic nephropathy, including chronickidney disease and end-stage renal fibrosis. The present study investigatedthe protective function of fucoidan in renal fibrosis and its pharmacologicalmechanism. The renal fibrotic model was established with the administrationof potassium oxonate for 10 weeks. The protein levels of related factorswere assessed in HUA mice by an enzyme-linked immunosorbent assay(ELISA) and western blotting. The results showed that fucoidan significantlyreduced the levels of serum uric acid, blood urea nitrogen (BUN),& alpha;-smooth muscle actin (& alpha;-SMA), and collagen I, and improvedkidney pathological changes. Furthermore, renal fibrosis had beenremarkably elevated through the inhibition of the epithelial-to-mesenchymaltransition (EMT) progression after fucoidan intervention, suppressingthe Janus kinase 2 (JAK2) signal transducer and activator of transcriptionprotein 3 (STAT3) signaling pathway activation. Together, this studyprovides experimental evidence that fucoidan may protect against hyperuricemia-inducedrenal fibrosis via downregulation of the JAK2/STAT3 signaling pathway.

Automated summary

This study found that fucoidan has a protective effect against hyperuricemia-induced renal fibrosis. It reduces serum uric acid levels, improves kidney pathology, and inhibits the progression of renal fibrosis by suppressing the epithelial-to-mesenchymal transition and the activation of the JAK2/STAT3 signaling pathway.