ReferenceID 2795
Rutaecarpine, an Alkaloid from Evodia rutaecarpa, Can Prevent Platelet Activation in Humans and Reduce Microvascular Thrombosis in Mice: Crucial Role of the PI3K/Akt/GSK3β Signal Axis through a Cyclic Nucleotides/VASP-Independent Mechanism
Int J Mol Sci
The role of activated platelets in acute and chronic cardiovascular diseases (CVDs) is well established. Therefore, antiplatelet drugs significantly reduce the risk of severe CVDs. Evodia rutaecarpa (Wu-Chu-Yu) is a well
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- Reference Id
- 2795
- Evidence Id
- 19385
- Core Evidence Id
- 19385
- Source Reference Id
- 5592
- Herb2 Reference Id
- HBREF006389
- Subject Paper Key
- HBIN042657_34681769
- Pubmed Id
- 34681769
- Doi
- 10.3390/ijms222011109
- Paper Title
- Rutaecarpine, an Alkaloid from Evodia rutaecarpa, Can Prevent Platelet Activation in Humans and Reduce Microvascular Thrombosis in Mice: Crucial Role of the PI3K/Akt/GSK3β Signal Axis through a Cyclic Nucleotides/VASP-Independent Mechanism
- Paper Abstract
- The role of activated platelets in acute and chronic cardiovascular diseases (CVDs) is well established. Therefore, antiplatelet drugs significantly reduce the risk of severe CVDs. Evodia rutaecarpa (Wu-Chu-Yu) is a well-known Chinese medicine, and rutaecarpine (Rut) is a main bioactive component with substantial beneficial properties including vasodilation. To address a research gap, we investigated the inhibitory mechanisms of Rut in washed human platelets and experimental mice. At low concentrations (1-5 muM), Rut strongly inhibited collagen-induced platelet aggregation, whereas it exerted only a slight or no effect on platelets stimulated with other agonists (e.g., thrombin). Rut markedly inhibited P-selectin expression; adenosine triphosphate release; [Ca2+]i mobilization; hydroxyl radical formation; and phospholipase C (PLC)gamma2/protein kinase C (PKC), mitogen-activated protein kinase, and phosphoinositide 3-kinase (PI3K)/Akt/glycogen synthase kinase-3beta (GSK3beta) phosphorylation stimulated by collagen. SQ22536 (an adenylate cyclase inhibitor) or ODQ (a guanylate cyclase inhibitor) did not reverse Rut-mediated antiplatelet aggregation. Rut was not directly responding to vasodilator-stimulated phosphoprotein phosphorylation. Rut significantly increased the occlusion time of fluorescence irradiated thrombotic platelet plug formation. The findings demonstrated that Rut exerts a strong effect against platelet activation through the PLCgamma2/PKC and PI3K/Akt/GSK3beta pathways. Thus, Rut can be a potential therapeutic agent for thromboembolic disorders.
- Journal
- Int J Mol Sci
- Publish Year
- 2021
- Experiment Subject
- mouse; human
- Experiment Type
- Animal Experiment
- Phenotype Related
- Acute And Chronic Cardiovascular Diseases; Thromboembolic Disorders; Cvds
- Paper Title Cn
- Paper Title En
- Rutaecarpine, an Alkaloid from Evodia rutaecarpa, Can Prevent Platelet Activation in Humans and Reduce Microvascular Thrombosis in Mice: Crucial Role of the PI3K/Akt/GSK3β Signal Axis through a Cyclic Nucleotides/VASP-Independent Mechanism
- Bilingual Status
- semi_complete