
Biomedicines, Journal Year: 2024, Volume and Issue: 12(12), P. 2847 - 2847
Published: Dec. 14, 2024
Background/Objectives: Fucoidan, a sulfated polysaccharide derived from marine algae, is known for its antioxidant and immunomodulatory properties. Galectin-3 (Gal-3), protein associated with cardiovascular fibrosis, has been identified as potential therapeutic target in cardiac remodeling. This study aimed to evaluate whether fucoidan could inhibit Gal-3 activity mitigate remodeling mouse model of pressure overload-induced hypertrophy. Methods: To test this hypothesis, we used transverse aortic constriction (TAC) surgery induce overload normotensive mice, replicating the pathological features Mice were treated at dose 1.5 or 7.5 mg/kg/day. In vivo assessments function, inflammation, expression performed. Results: Pressure led significant upregulation serum levels, increased collagen deposition, elevated markers fibrosis inflammation. mice fucoidan, these effects significantly attenuated. Fucoidan treatment prevented Gal-3, reduced decreased inflammatory cell infiltration, suggesting an inhibition both Conclusions: effectively mitigated adverse model, including expression, These findings suggest that holds promise agent preventing delaying complications, such Further research needed explore underlying mechanisms clinical applicability disease.
Language: Английский