ABSTRACT
Fucoidan is a native sulfated polysaccharide mainly isolated from brown seaweed, with diverse pharmacological activities, such as anti-inflammatory and antifibrosis. Hyperuricemia (HUA) is a common metabolic disease worldwide and mainly causes hyperuricemic nephropathy, including chronic kidney disease and end-stage renal fibrosis. The present study investigated the protective function of fucoidan in renal fibrosis and its pharmacological mechanism. The renal fibrotic model was established with the administration of potassium oxonate for 10 weeks. The protein levels of related factors were assessed in HUA mice by an enzyme-linked immunosorbent assay (ELISA) and western blotting. The results showed that fucoidan significantly reduced the levels of serum uric acid, blood urea nitrogen (BUN), α-smooth muscle actin (α-SMA), and collagen I, and improved kidney pathological changes. Furthermore, renal fibrosis had been remarkably elevated through the inhibition of the epithelial-to-mesenchymal transition (EMT) progression after fucoidan intervention, suppressing the Janus kinase 2 (JAK2) signal transducer and activator of transcription protein 3 (STAT3) signaling pathway activation. Together, this study provides experimental evidence that fucoidan may protect against hyperuricemia-induced renal fibrosis via downregulation of the JAK2/STAT3 signaling pathway.
Subject(s)
Hyperuricemia , Laminaria , Renal Insufficiency, Chronic , Mice , Animals , Janus Kinase 2/genetics , Janus Kinase 2/metabolism , Uric Acid/metabolism , Laminaria/metabolism , Kidney/metabolism , Fibrosis , Polysaccharides/metabolism , Signal Transduction , Renal Insufficiency, Chronic/metabolismABSTRACT
Fucoxanthin is a major marine carotenoid with many biological activities. It is well known that fucoxanthin is unstable to heat and acid due to its polyunsaturated structure. Another defect of fucoxanthin is the low bioavailability and all these drawbacks make it limited in the food industry. In order to improve its stability and intestinal absorption, fucoxanthin was encapsulated with biopolymers by spray drying in this study. All the microspheres we prepared had a spherical shape with encapsulation efficiencies (EE) ranging from 86.48% to 97.06%. A heat stability test showed that maltodextrin (MD), gum arabic (GA) and whey protein isolate (WPI) improved the thermal stability of fucoxanthin. The degradation kinetics of the loaded fucoxanthin encapsulated with biopolymers also indicated that GA and MD had a better protective effect on fucoxanthin. The encapsulated fucoxanthin degradation rate within MD, GA, WPI and gelatin (GEL) followed second-order kinetics and their half-life (t 1/2) was 92.6 d, 99.8 d, 50.9 d and 69.3 d, respectively. The simulated digestion test in vitro suggested that MD, GA and WPI effectively protected fucoxanthin in the gastric acid environment, meanwhile increasing the release rate of fucoxanthin in the intestinal tract.
