Dioscin from smilax china rhizomes inhibits platelet activation and thrombus formation via up-regulating cyclic nucleotides
Abstract Cardiovascular disease, the leading cause of mortality in the United States, is caused by abnormal platelet accumulation and coagulation. Dioscin has been reported to suppress the growth of tumor-associated cells and trigger apoptosis. However, its mechanism in inhibiting platelet activatio...
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Nature Portfolio
2025-07-01
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| Series: | Scientific Reports |
| Online Access: | https://doi.org/10.1038/s41598-025-09452-7 |
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| author | Ga Hee Lee Jin Pyo Lee Na Yoon Heo Chang-Dae Lee Gyeongchan Kim Akram Abdul Wahab Man Hee Rhee Sanghyun Lee Dong-Ha Lee |
| author_facet | Ga Hee Lee Jin Pyo Lee Na Yoon Heo Chang-Dae Lee Gyeongchan Kim Akram Abdul Wahab Man Hee Rhee Sanghyun Lee Dong-Ha Lee |
| author_sort | Ga Hee Lee |
| collection | DOAJ |
| description | Abstract Cardiovascular disease, the leading cause of mortality in the United States, is caused by abnormal platelet accumulation and coagulation. Dioscin has been reported to suppress the growth of tumor-associated cells and trigger apoptosis. However, its mechanism in inhibiting platelet activation has not been confirmed. This study investigates whether dioscin from Smilax china rhizomes exerts antithrombotic effects by regulating the activation of human platelets and explains its mechanism of action. Dioscin increased the production of cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP). This increase induced the phosphorylation of inositol 1,4,5-triphosphate receptor (IP3R), which inhibited the dense Ca2+ release channels, thereby reducing Ca2+ mobilization. Furthermore, it promoted the phosphorylation of vasodilator-stimulated phosphoprotein (VASP), which suppressed integrin αIIbβ3 and fibrinogen binding, thus inhibiting platelet activation. Dioscin regulated phosphorylation of phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt), mitogen-activated protein kinase (MAPK) and cytosolic phospholipase A2 (cPLA2), which are proteins associated with platelet granule release. Finally, ingestion of S. china rhizomes containing dioscin significantly inhibited thrombus formation in the FeCl3-induced thrombosis model. Therefore, dioscin from S. china rhizomes exhibited antiplatelet effects that could delay or halt thrombus formation by regulating the phosphorylation of various signaling molecules and related proteins, thus suggesting dioscin’s potential value for development as an antithrombotic agent. |
| format | Article |
| id | doaj-art-21ea9b59318d45fa89f8e25fb67b1e73 |
| institution | DOAJ |
| issn | 2045-2322 |
| language | English |
| publishDate | 2025-07-01 |
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| spelling | doaj-art-21ea9b59318d45fa89f8e25fb67b1e732025-08-20T03:04:30ZengNature PortfolioScientific Reports2045-23222025-07-0115111410.1038/s41598-025-09452-7Dioscin from smilax china rhizomes inhibits platelet activation and thrombus formation via up-regulating cyclic nucleotidesGa Hee Lee0Jin Pyo Lee1Na Yoon Heo2Chang-Dae Lee3Gyeongchan Kim4Akram Abdul Wahab5Man Hee Rhee6Sanghyun Lee7Dong-Ha Lee8Department of Biomedical Laboratory Science, Namseoul UniversityDepartment of Biomedical Laboratory Science, Namseoul UniversityDepartment of Biomedical Laboratory Science, Namseoul UniversityDepartment of Plant Science and Technology, Chung-Ang UniversityDepartment of Health Administration and Management, Soonchunhyang University Graduate SchoolDepartment of Veterinary Medicine, College of Veterinary Medicine, Kyungpook National UniversityDepartment of Veterinary Medicine, College of Veterinary Medicine, Kyungpook National UniversityDepartment of Plant Science and Technology, Chung-Ang UniversityDepartment of Biomedical Laboratory Science, Namseoul UniversityAbstract Cardiovascular disease, the leading cause of mortality in the United States, is caused by abnormal platelet accumulation and coagulation. Dioscin has been reported to suppress the growth of tumor-associated cells and trigger apoptosis. However, its mechanism in inhibiting platelet activation has not been confirmed. This study investigates whether dioscin from Smilax china rhizomes exerts antithrombotic effects by regulating the activation of human platelets and explains its mechanism of action. Dioscin increased the production of cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP). This increase induced the phosphorylation of inositol 1,4,5-triphosphate receptor (IP3R), which inhibited the dense Ca2+ release channels, thereby reducing Ca2+ mobilization. Furthermore, it promoted the phosphorylation of vasodilator-stimulated phosphoprotein (VASP), which suppressed integrin αIIbβ3 and fibrinogen binding, thus inhibiting platelet activation. Dioscin regulated phosphorylation of phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt), mitogen-activated protein kinase (MAPK) and cytosolic phospholipase A2 (cPLA2), which are proteins associated with platelet granule release. Finally, ingestion of S. china rhizomes containing dioscin significantly inhibited thrombus formation in the FeCl3-induced thrombosis model. Therefore, dioscin from S. china rhizomes exhibited antiplatelet effects that could delay or halt thrombus formation by regulating the phosphorylation of various signaling molecules and related proteins, thus suggesting dioscin’s potential value for development as an antithrombotic agent.https://doi.org/10.1038/s41598-025-09452-7 |
| spellingShingle | Ga Hee Lee Jin Pyo Lee Na Yoon Heo Chang-Dae Lee Gyeongchan Kim Akram Abdul Wahab Man Hee Rhee Sanghyun Lee Dong-Ha Lee Dioscin from smilax china rhizomes inhibits platelet activation and thrombus formation via up-regulating cyclic nucleotides Scientific Reports |
| title | Dioscin from smilax china rhizomes inhibits platelet activation and thrombus formation via up-regulating cyclic nucleotides |
| title_full | Dioscin from smilax china rhizomes inhibits platelet activation and thrombus formation via up-regulating cyclic nucleotides |
| title_fullStr | Dioscin from smilax china rhizomes inhibits platelet activation and thrombus formation via up-regulating cyclic nucleotides |
| title_full_unstemmed | Dioscin from smilax china rhizomes inhibits platelet activation and thrombus formation via up-regulating cyclic nucleotides |
| title_short | Dioscin from smilax china rhizomes inhibits platelet activation and thrombus formation via up-regulating cyclic nucleotides |
| title_sort | dioscin from smilax china rhizomes inhibits platelet activation and thrombus formation via up regulating cyclic nucleotides |
| url | https://doi.org/10.1038/s41598-025-09452-7 |
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