University Presentation Showcase: Undergraduate Division

Vasicine as a Modulator of Thrombin-Induced Clotting

Presenter Hometown

Somerset, KY

Major

Biomedical Science, Pre-Med Concentration

Department

Biological Sciences

Degree

Undergraduate

Mentor

Dr. Smita Joshi

Mentor Department

Biological Sciences

Abstract

Background: Cardiovascular diseases (CVDs) remain the leading global cause of death, driven largely by thrombotic complications. The Commonwealth of Kentucky ranks 48th in the nation for cardiovascular health, underlining the urgency for better treatments and resources to address this burden. The underlying cause of many CVDs is hyperactive platelets that lead to occlusive clot formation, causing myocardial infarctions and strokes. Current anti-platelet therapies frequently induce excessive bleeding, necessitating the discovery of alternative agents that modulate platelet activity without compromising hemostasis. The quinazoline alkaloid vasicine, the primary bioactive component of the medicinal plant Adhatoda vasica, possesses anti-inflammatory properties and is implicated in platelet inhibition; however, its pharmacological mechanism of action remains undefined.

Objective: This ongoing project aims to systematically evaluate the dose-dependent effects of vasicine on platelet function and coagulation.

Methods: Platelets isolated via centrifugation were treated with varying concentrations of vasicine and subsequently activated using different concentrations of thrombin. Aggregation responses were recorded via lumi-aggregometry. To determine how vasicine affects coagulation, an absorbance-based plate assay was performed.

Results: Initial experimental trials indicate that vasicine inhibits thrombin-induced platelet aggregation. Reconstituted human plasma treated with vasicine demonstrated decreased fibrin formation and accelerated lysis.

Conclusion: Preliminary data indicate that vasicine exhibits both antiplatelet and anticoagulant properties. Further mechanistic studies are required to elucidate the molecular targets underlying vasicine’s function.

Research reported in this project was supported by the National Institute of General Medical Sciences of the National Institutes of Health under Award Number P20GM103436.

Presentation format

Poster

This document is currently not available here.

Share

COinS
 

Vasicine as a Modulator of Thrombin-Induced Clotting

Background: Cardiovascular diseases (CVDs) remain the leading global cause of death, driven largely by thrombotic complications. The Commonwealth of Kentucky ranks 48th in the nation for cardiovascular health, underlining the urgency for better treatments and resources to address this burden. The underlying cause of many CVDs is hyperactive platelets that lead to occlusive clot formation, causing myocardial infarctions and strokes. Current anti-platelet therapies frequently induce excessive bleeding, necessitating the discovery of alternative agents that modulate platelet activity without compromising hemostasis. The quinazoline alkaloid vasicine, the primary bioactive component of the medicinal plant Adhatoda vasica, possesses anti-inflammatory properties and is implicated in platelet inhibition; however, its pharmacological mechanism of action remains undefined.

Objective: This ongoing project aims to systematically evaluate the dose-dependent effects of vasicine on platelet function and coagulation.

Methods: Platelets isolated via centrifugation were treated with varying concentrations of vasicine and subsequently activated using different concentrations of thrombin. Aggregation responses were recorded via lumi-aggregometry. To determine how vasicine affects coagulation, an absorbance-based plate assay was performed.

Results: Initial experimental trials indicate that vasicine inhibits thrombin-induced platelet aggregation. Reconstituted human plasma treated with vasicine demonstrated decreased fibrin formation and accelerated lysis.

Conclusion: Preliminary data indicate that vasicine exhibits both antiplatelet and anticoagulant properties. Further mechanistic studies are required to elucidate the molecular targets underlying vasicine’s function.

Research reported in this project was supported by the National Institute of General Medical Sciences of the National Institutes of Health under Award Number P20GM103436.