Effect of Fucoidan on NF-κB-Mediated Inflammatory Response in Rats with Acute Myocardial Infarction

Abstract

The incidence of cardiovascular disease in China has been increased year by year. Studies have suggested that fucoidan has many biological activities such as anti-coagulation, anti-tumor and anti-thrombosis. However, the effect of fucoidan on acute myocardial infarction (AMI) is unclear. In this study, a rat model of AMI was made by coronary artery ligation. The NF-κB inhibitor PDTC or fucoidan intervention was administered followed by analysis of the degree of pathological damage of myocardial infarction by hematoxylin-eosin (HE) staining, the expression of related proteins by Western blot, and the level of myocardial enzyme and inflammation by ELISA kit. Severe myocardial damage was observed in rats in the myocardial infarction model group, which was improved in both PDTC and fucoidan groups. At the same time, NF-κB signaling was significantly activated in the myocardial infarction model group. Both PDTC and fucoidan could inhibit NF-κB signaling activation and reduce the secretion of TNF-α and IL-6. Administration of PDTC and fucoidan also improved myocardial enzymes and decreased level of aspartate aminotransferase (AST), creatine kinase (CK), and creatine kinase isoenzyme (CKMB). Fucoidan can inhibit NF-κB-mediated inflammation and improve myocardial injury in rats with acute myocardial infarction, which provides a theoretical basis for the development of anti-infarction drugs for treating AMI.