American Society of Hirudotherapy

Antithrombotic effects of saratin on human atherosclerotic plaques

Research article published in Thromb Haemost (2004)

Last Updated: June 18, 2026Reviewed by: ASH Editorial Board
Research article — evidence reviewArticle reference
Evidence: Research reportSalivary PharmacologyDrug DevelopmentVilahur G et al. · Thromb Haemost, 2004

Abstract

Platelets play a primary role in thrombus formation after plaque rupture. Platelets recognize the exposed collagen via Von Willebrand factor (VWF) and become activated. Saratin, an inhibitor of the VWF-dependent binding of platelets to collagen, may reduce the thrombotic risk associated to atherosclerosis. Our objective was to evaluate the antithrombotic effects of local treatment with saratin on human atherosclerotic lesions. Thrombus formation was assessed by the deposition of (111)In-platelets on different human atherosclerotic lesions under three local shear conditions (800,1700 and 3400/s) with blood derived from catheterized pigs. Human atherosclerotic lesions were locally treated with saratin (30 microg/ml) at 37 degrees C for 5 min and placed in the chamber. Under stenotic shear conditions of 800/s, saratin significantly (p<0.05) reduced platelet deposition triggered by human denuded vessel wall (44%), fatty streaks (47%), severely damaged vessel (50%) and atherosclerotic plaque (57%). Thrombus characterization by immunohistochemistry showed also a reduction in fibrin deposition in treat-ed vessels. These results suggest that the local site-specific treatment with saratin inhibits atherosclerotic plaque thrombogenicity at haemodynamic conditions typical of moderately stenotic coronary arteries.

Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.

Publication typeJournal ArticleResearch Support, Non-U.S. Gov't
Indexed MeSH termsAnimalsArteriosclerosisBlood PlateletsCollagenFibrinolytic AgentsHumansIn Vitro TechniquesIndium RadioisotopesPlatelet AdhesivenessSalivary Proteins and PeptidesSus scrofaThrombosis

Summary

Platelets play a primary role in thrombus formation after plaque rupture. Platelets recognize the exposed collagen via Von Willebrand factor (VWF) and become activated.

Why This Matters for Hirudotherapy

This study assessed whether local treatment with saratin—an inhibitor of VWF-dependent platelet binding to collagen—reduced thrombus formation on human atherosclerotic lesions perfused with catheterized-pig blood under controlled shear conditions (800–3400/s). Saratin is a bioactive peptide derived from the medicinal leech secretome, so this work directly illustrates how a leech-derived antithrombotic factor may counteract plaque-triggered thrombosis, connecting core hirudotherapy science to a major vascular disease mechanism relevant to ASH members. At stenotic shear (800/s), saratin (30 µg/ml) significantly reduced platelet deposition across lesion types (44–57%) and decreased fibrin deposition in treated vessels. The key caveat is that this experimental perfusion model used porcine blood and measured acute platelet and fibrin endpoints, not clinical outcomes in human patients, so therapeutic efficacy remains unproven beyond this controlled setting.

Citation

Antithrombotic effects of saratin on human atherosclerotic plaques.

Vilahur G et al. · Thromb Haemost, 2004

DOI

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