4.6 Article

A Novel Polysaccharide from Auricularia Auricula Alleviates Thrombosis Induced by Carrageenan in Mice

期刊

MOLECULES
卷 27, 期 15, 页码 -

出版社

MDPI
DOI: 10.3390/molecules27154831

关键词

Auricularia auricula; polysaccharide; structure elucidation; antithrombotic activity; thrombosis

资金

  1. National Natural Science Foundation of China [31801485]
  2. Natural Science Foundation of Heilongjiang Province [LH2020C064]
  3. Startup Foundation for Youth Doctoral Scientific Research of Harbin University [HUDF2020104]

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This study revealed that the polysaccharide AAP-b2 isolated from Auricularia auricula fruiting bodies exhibited significant antithrombotic activity by inhibiting platelet aggregation and thrombus formation, as well as enhancing anticoagulant mechanisms.
The increasing incidence of cardiovascular diseases has created an urgent need for safe and effective antithrombotic agents. In this study, we aimed to elucidate the structural characteristics and antithrombotic activity of a novel polysaccharide isolated from Auricularia auricula fruiting bodies. The purified polysaccharide AAP-b2 (12.02 kDa) was composed of mannose, glucuronic acid, glucose and xylose, with a molar ratio of 89.25:30.50:4.25:1.00. Methylation and NMR analyses showed that AAP-b2 primarily consisted of -> 2,3)-Manp-(1 ->, -> 3)-Manp-(1 ->, -> 4)-GlcAp-(1 -> and Manp-(1 ->. A thrombus mouse model induced by carrageenan was used in this research to evaluate its antithrombotic effect. AAP-b2 significantly inhibited platelet aggregation, reduced the black tail length and prolonged the coagulation time, including activated partial thromboplastin time (APTT), prothrombin time (PT) and thrombin time (TT), exerting a good inhibitory effect on thrombosis in mice. The antithrombotic activity of AAP-b2 was found to be related to the inhibition of platelet activation by regulation of endothelial nitric oxide synthases (eNOs), endothelin-1 (ET-1), prostacyclin (PGI2) and thromboxane B2 (TXB2), along with the enhancement of anticoagulant activity by affecting antithrombin III (AT-III) and protein C (PC) pathways.

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