Fucoidan, a sulfated polysaccharide from brown algae, against myocardial ischemia-reperfusion injury in rats via regulating the inflammation response

The aim of the study was to determine the effects of fucoidan on rat myocardial ischemia-reperfusion (I/R) model and elucidate the potential mechanisms. Myocardial I/R injury was induced by the occlusion of left anterior descending coronary artery for 30 min followed by reperfusion for 2 h. After 2 h reperfusion, hemodynamics parameters were detected. Blood samples were collected to determine serum levels of tumor necrosis factor-alpha (TNF-alpha) and interleukin 6, 10 (IL-6, 10). Hearts were harvested to assess histopathological changes, infarct size (IS), and the content of myeloperoxidase (MPO). The expression of high-mobility group box 1 (HMGB1), phosphor-I kappa beta-alpha and phosphor-nuclear factor kappa B (NF-kappa B) were assayed by western blot. Compared with control group, treatment with fucoidan improved left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP) and the contractility index (P < 0.05, P < 0.01). Fucoidan reduced the myocardial IS, the levels of TNF-alpha and IL-6, and the activity of MPO (P < 0.05, P < 0.01). Fucoidan down-regulated the expression of HMGB1, phosphor-I kappa beta-alpha and NF-kappa B, but increased the content of IL-10 when compared with control (P < 0.05, P < 0.01). Besides, the infiltration of polymorph nuclear leukocytes (PMNs) and histopathological damages in myocardium were decreased in fucoidan treated groups (PMNs, P < 0.05, P < 0.01). These findings revealed that the administration of fucoidan could regulate the inflammation response via HMGB1 and NF-kappa B inactivation in I/R-induced myocardial damage. (C) 2011 Elsevier Ltd. All rights reserved.