Qiliqiangxin capsule attenuates platelet activation and thrombosis by suppressing Ca2+ influx and PKC signaling

Sep 29, 2026

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Arterial thrombotic diseases remain major global causes of morbidity and mortality driven by platelet hyperactivity. Qiliqiangxin capsules (QLQX), a Chinese medicine approved for heart failure, show potential cardiovascular benefit, yet direct effects on platelet activation and thrombosis were unclear. Ex vivo and in vivo experiments show that QLQX inhibits agonist-induced platelet aggregation, spreading, clot retraction, and thrombus formation while suppressing Ca2+ influx and PKC signaling without increasing bleeding.

LanguageEnglish

CategoryHealthcare

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Abstract

Background

Methods and results

Conclusion

Introduction

Han et al. Thrombosis Journal (2026) 24:2 Thrombosis Journal [https://doi.org/10.1186/s12959-025-00823-8](https://doi.org/10.1186/s12959-025-00823-8) RESEARCH Open Access Qiliqiangxin capsule attenuates platelet activation and thrombosis by suppressing Ca2+ influx and PKC signaling Liping Han 1,3†, Wei Zhang2,3†, Changyu Huo3, Anqi Zhou3, Ziru Huang3, Yanqi Wang3, Biwei Yang5, Lihua Cao6, Si Zhang2,3, Jiayu Zheng4* and Rong Xia 1* Abstract Background Arterial thrombotic diseases are leading causes of global morbidity and mortality, primarily driven by platelet hyperactivity. Qiliqiangxin capsules (QLQX), a traditional Chinese medicine approved in China for the treatment of heart failure, have exhibited potential benefits in reducing cardiovascular death. However, its direct effects on platelet activation and thrombosis remain unclear. Methods and results Ex vivo platelet function assays demonstrated that oral QLQX inhibited agonist-induced aggregation in platelet-rich plasma (PRP) from chronic heart failure (CHF) patients and dose-dependently suppressed washed platelet aggregation in wild-type mice. In parallel, QLQX administration attenuated platelet spreading and clot retraction in washed platelets from both patients with CHF and wild-type mice, and reduced ex vivo thrombus formation area in a microfluidic whole-blood perfusion under arterial shear stress. Flow cytometry analysis revealed that QLQX did not affect the surface expression levels of the major platelet receptors, but reduced the activation of αIIbβ3 and P-selectin exposure induced by thrombin in mouse platelets. In vivo experiments demonstrated that QLQX treatment inhibited FeCl₃-induced thrombus formation in mesenteric arterioles, reduced collagen/epinephrineinduced pulmonary embolism, and mitigated microvascular thrombosis during myocardial ischemia-reperfusion (I/R) injury, without increasing bleeding in mice. RNA sequencing of platelets from QLQX-versus vehicle-treated mice identified differential ly expressed genes enriched in the calcium signaling pathway, and functional assays demonstrated that QLQX inhibited agonist-induced platelet Ca²⁺ influx and PKC phosphorylation. Conclusion QLQX inhibits platelet activation and thrombosis by targeting Ca²⁺ influx and PKC signaling, supporting its potential therapeutic value in preventing thrombotic complications. Keywords Platelet activation, Qiliqiangxin capsules, Thrombosis †Liping Han and Wei Zhang joint first author. *Correspondence: Jiayu Zheng [zheng.jiayu@zs-hospital.sh.cn](zheng.jiayu@zs-hospital.sh.cn)[ ](zheng.jiayu@zs-hospital.sh.cn)Rong Xia [rongxia@fudan.edu.cn](rongxia@fudan.edu.cn) 1Department of Transfusion Medicine, Huashan Hospital, Fudan University, Shanghai 200040, China 2Department of Hematology, Zhongshan Hospital Qingpu Branch, Fudan University, Shanghai 200032, China 3NHC Key Laboratory of Glycoconjugate Research, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China 4Department of Cardiac Surgery, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai 200032, China 5Liver Cancer Institute, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai 200032, China 6Liver Cancer Institute, Qidong People‘s Hospital Affiliated to Nantong University, Nantong 226200, China © The Author(s) 2025. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Com

FAQs

What problem does the study address regarding arterial thrombosis?

The study targets arterial thrombotic diseases, where platelet hyperreactivity is a central driver of thrombosis and contributes to high morbidity and mortality.

How does Qiliqiangxin capsule (QLQX) affect platelet function in experiments?

Ex vivo assays show QLQX inhibits agonist-induced aggregation and reduces platelet spreading and clot retraction, along with decreased ex vivo thrombus formation under arterial shear stress.

What mechanism is proposed for QLQX’s antithrombotic effects?

QLQX does not change major platelet receptor surface expression but reduces thrombin-induced activation markers and inhibits agonist-induced platelet Ca2+ influx and PKC phosphorylation.

Sep 29, 2026

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