PB0894 - Investigating the antiplatelet potential of Chrysotoxine in human platelets: A multi-target approach

Monday, June 24, 2024

13:45 – 14:45 ICT

Room: Exhibition Hall

Co-Author(s)

HS

Hla Nu Swe

Postgraduate student
Pharmaceutical Sciences and Technology Program, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok 10330 Thailand
Bangkok, Krung Thep, Thailand

Presenting Author(s)

Fozia Rustamani, PharmD, MPhil

PhD Scholar
Pharmaceutical Sciences and Technology Program, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok 10330 Thailand
Bangkok, Krung Thep, Thailand

Co-Author(s)

NN

Nonthaneth Nalinratana

Lecturer
Department of Pharmacology and Physiology, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok 10330 Thailand
Bangkok, Krung Thep, Thailand
BS

Boonchoo Sritularak

Associate Professor
Department of Pharmacognosy and Pharmaceutical Botany, Faculty of Pharmaceutical Sciences, Chulalongkorn University, Bangkok 10330, Thailand
Bangkok, Krung Thep, Thailand
Ponlapat Rojnuckarin, MD, PhD

Professor
Excellence Center in Translational Hematology, Department of Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand
Bangkok, Krung Thep, Thailand
RL

Rataya Luechapudiporn

Associate Professor
Department of Pharmacology and Physiology, Faculty of Pharmaceutical Sciences, Chulalongkorn University
Bangkok, Krung Thep, Thailand

Background: Cardiovascular diseases cause morbidity and mortality globally. Conventional antithrombotic therapy when used alone may yield treatment failure due to a single target and/or bleeding complications due to high potency or combined therapy. Chrysotoxine, a bibenzyl isolated from orchids of Dendrobium spp., exhibits definite multi-target inhibitory effects, and can serve as a promising lead compound for investigating multi-target inhibitors.

Aims: We investigated the effects of chrysotoxine on platelet aggregation and cytotoxicity on EA.hy926 endothelial cell culture.

Methods: The anti-platelet activity of chrysotoxine on platelet aggregation induced by adenosine diphosphate (ADP), arachidonic acid (AA), and collagen in human platelet-rich plasma (PRP) was measured using the Born turbidimetric aggregometer. Aspirin was used as a positive control. The platelets were collected from healthy volunteers after informed consent and approval by the Institutional Review Board at the Faculty of Medicine, Chulalongkorn University. Additionally, we assessed the non-toxic concentration of chrysotoxine on the human umbilical vein cell line, EA.hy926, using the MTT assay.

Results: In vitro, chrysotoxine significantly inhibited ADP-, AA-, and collagen-induced platelet aggregation with the half maximal inhibitory concentrations (IC50) of 0.27 mM, 0.126 mM, and 0.41 mM, respectively, in a dose-dependent manner (figure 1). On the other hand, chrysotoxine exhibited no cytotoxicity on endothelial cells in concentrations ranging from 1 to 200 μM.

Conclusion(s): Our study demonstrates that chrysotoxine exhibits potent antiplatelet effects without inducing cytotoxicity in endothelial cells. The platelet inhibitory activities against ADP, AA, and collagen suggest its potential therapeutic relevance. Further research is needed to investigate the underlying molecular mechanisms and explore its vasoprotective effects, opening avenues for potential therapeutic applications in cardiovascular disorders.