Conclusions
Fucoidan effectively mitigated the adverse effects of pressure overload in this mouse model, including reduced Gal-3 expression, fibrosis, and inflammation. These findings suggest that fucoidan holds promise as a therapeutic agent for preventing or delaying cardiac remodeling and associated complications, such as fibrosis and inflammation, in pressure overload-induced cardiac hypertrophy. Further research is needed to explore the underlying mechanisms and clinical applicability of fucoidan in cardiac disease.
Methods
To test this hypothesis, we used transverse aortic constriction (TAC) surgery to induce pressure overload in normotensive mice, replicating the pathological features of cardiac hypertrophy. Mice were treated with fucoidan at a dose of 1.5 or 7.5 mg/kg/day. In vivo assessments of cardiac function, fibrosis, inflammation, and Gal-3 expression were performed.
Results
Pressure overload led to significant upregulation of serum Gal-3 levels, increased cardiac collagen deposition, and elevated markers of fibrosis and inflammation. In mice treated with fucoidan, these effects were significantly attenuated. Fucoidan treatment prevented the upregulation of Gal-3, reduced collagen deposition, and decreased inflammatory cell infiltration, suggesting an inhibition of both fibrosis and inflammation. Conclusions: Fucoidan effectively mitigated the adverse effects of pressure overload in this mouse model, including reduced Gal-3 expression, fibrosis, and inflammation. These findings suggest that fucoidan holds promise as a therapeutic agent for preventing or delaying cardiac remodeling and associated complications, such as fibrosis and inflammation, in pressure overload-induced cardiac hypertrophy. Further research is needed to explore the underlying mechanisms and clinical applicability of fucoidan in cardiac disease.