Abstract: Objective: To investigate whether fucoidan could improve cardiac function and attenuate inflammation after myocardial infarction (MI) in mice. Method: Mice were randomly divided into sham group, myocardial infarction model group (left anterior descending coronary artery ligation), low or high concentrations fucoidan-treated group (mice were gavaged 200mg/kg or 500mg/kg fucoidan daily after surgery). Mice were observed daily for death. Three weeks later echocardiography was used to detect cardiac function. pathology staining was used to detect infarct size and RT-PCR to measure the mRNA expression levels of SOD, inducible nitric oxide synthase (iNOS) and inflammatory cytokines TNFα, IL -1β and TGFβ. Western blot was used to detect the eNOS signaling pathway. Results: After treatment for 3 weeks, Fucoidan could increase survival rate (p＜0.05), improve heart function (p＜0.05) and decrease infarct size (p＜0.05) compared with vehicle. Moreover, Fucoidan could down-regulate the mRNA expression of some inflammatory cytokines such as TNFα, IL-1β, TGFβ (p＜0.05) and activate eNOS pathway. Conclusion: Fucoidan can reduce inflammation, and improve cardiac function after ischemic injury. It represents a potential novel therapeutic approach for treatment of ischemic heart disease.

Key words: Fucoidan, myocardial infraction, inflammation, anti-oxidative, eNOS