Journal
INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
Volume 126, Issue -, Pages 179-186Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.ijbiomac.2018.12.207
Keywords
Astragalus polysaccharide from Astragalus; Melittin; Virus myocarditis; Inflammation; TLR-4/NF-kappa B p65 signal pathway
Funding
- National Natural Science Foundation of China [81460066]
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Inflammation plays a crucial role in regulating cardiomyopathy and injuries of coxsackievirus B3 (CVB3)-induced viral myocarditis (VM). It has been reported that Astragalus polysaccharide (AP) from Astragalus Melittin could inhabit inflammatory gene expression under a variety of pathological conditions. However, the functional roles of AP in CVB3-induced VM still remain unknown. Here, we found that AP significantly enhanced survival for CVB3-induced mice. AP protected the mice against CVB3-induced myocardial injuries characterized by the increased body weight and depressed serum level of creatine kinase-MB (CK-MB), aspartate transaminases (AST) and lactate dehydrogenase (LDH), enhanced left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS). At the pathological level, AP ameliorated the mice against CVB3-induced myocardial damage, dilated cardiomyopathy and chronic myocardial fibrosis. We subsequently found that AP significantly suppressed CVB3-induced expression of inflammation marker (IL-1 beta, IL-6, TNF-alpha, INF-gamma and MCP-1) in heart. Furthermore, we confirmed that AP suppressed the CVB3-induced expression of TLR-4 and phosphorylated NF-kappa B p65 in heart. Taken together, the data suggest that AP protects against CVB3-induced myocardial damage and inflammation, which may partly attribute to the regulation of TLR-4/NF-kappa B p65 signal pathway, moreover, suppressive effect of AP on CVB3-induced activation of TLR-4/NF-kappa B p65 signal was TNF-alpha-independent. (C) 2018 Published by Elsevier B.V.
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