Rhamnan sulfate extracted from Monostroma nitidum attenuates blood coagulation and inflammation of vascular endothelial cells

• Published in: Journal of natural medicines Vol. 73; no. 3; pp. 614 - 619
• Main Authors: Okamoto, Takayuki, Akita, Nobuyuki, Terasawa, Masahiro, Hayashi, Tatsuya, Suzuki, Koji
• Format: Journal Article
• Language: English
• Published: Singapore Springer Singapore 01.06.2019; Springer Nature B.V
• Subjects: Algae; Anticoagulants; Anticoagulants - pharmacology; Anticoagulants - therapeutic use; Biomedical and Life Sciences; Biomedicine; Blood Coagulation - drug effects; Complementary & Alternative Medicine; Deoxy Sugars - pharmacology; Deoxy Sugars - therapeutic use; Endothelial Cells - drug effects; Endothelium; Herbal medicine; Humans; Inflammation; Inflammation - drug therapy; Lipopolysaccharides; Mannans - pharmacology; Mannans - therapeutic use; Medicinal Chemistry; Nitric oxide; Pharmacology/Toxicology; Pharmacy; Phytochemicals; Plant Sciences; Seaweed - drug effects; Sulfates - pharmacology; Sulfates - therapeutic use; Seaweed; Rhamnan sulfate; Vascular endothelium; Anti-coagulation; Anti-inflammation; Monostroma nitidum
• ISSN: 1340-3443; 1861-0293
• DOI: 10.1007/s11418-019-01289-5

Rhamnan sulfate (RS) is a polysaccharide with a rhamnose backbone isolated from Monostroma nitidum . Like heparin, it exerts anticoagulant activity in the presence of antithrombin. Endothelial cells facilitate the crosstalk between blood coagulation and vascular inflammation. In this study, we compared the effect of RS with that of heparin on blood coagulation and vascular endothelial cells in the presence or absence of inflammatory factors, using human umbilical vein endothelial cells. We found that RS significantly enhances inhibition of thrombin and factor Xa in the presence of antithrombin as well as heparin, and that RS inhibits tissue factor expression and von Willebrand factor release from the endothelial cells treated with or without lipopolysaccharide, tumor necrosis factor-α, or thrombin. Heparin did not show any effects on endothelial cell inflammation. Our findings suggest that RS, like heparin, is an antithrombin-dependent anticoagulant and, unlike heparin, is a potent anti-inflammatory agent acting on vascular endothelial cells.