American Society of Hirudotherapy

Recombinant hirudin suppresses angiogenesis of diffuselarge B-cell lymphoma through regulation of the PAR-1-VEGF

Research article published in Chemical biology & drug design (2024)

Last Updated: June 18, 2026Reviewed by: ASH Editorial Board
Research article — evidence reviewArticle reference
Evidence: Research reportDrug DevelopmentSalivary PharmacologyZhao J et al. · Chemical biology & drug design, 2024

Abstract

Hirudin is one of the specific inhibitors of thrombin, which has been confirmed to have strong bioactivities, including inhibiting tumors. However, the function and mechanism of hirudin and protease-activated receptor 1 (PAR-1) in diffuse large B-cell lymphoma (DLBCL) have not been clear. Detecting the expression PAR-1 in DLBCL tissues and cells by RT-qPCR and IHC. Transfected sh-NC, sh-PAR-1, or pcDNA3.1-PAR-1 in DLBCL cells or processed DLBCL cells through added thrombin, Vorapaxar, Recombinant hirudin (RH), or Na2S2O4 and co-culture with EA.hy926. And built DLBCL mice observed tumor growth. Detecting the expression of related genes by RT-qPCR, Western blot, IHC, and immunofluorescence, measured the cellular hypoxia with Hypoxyprobe-1 Kit, and estimated the cell inflammatory factors, proliferation, migration, invasion, and apoptosis by ELISA, CCK-8, flow cytometry, wound-healing and Transwell. Co-immunoprecipitation and pull-down measurement were used to verify the relationship. PAR-1 was highly expressed in DLBCL tissues and cells, especially in SUDHL2. Na2S2O4 induced SUDHL2 hypoxia, and PAR-1 did not influence thrombin-activated hypoxia. PAR-1 could promote SUDHL2 proliferation, migration, and invasion, and it was unrelated to cellular hypoxia. PAR-1 promoted proliferation, migration, and angiogenesis of EA.hy926 or SUDHL2 through up-regulation vascular endothelial growth factor (VEGF). RH inhibited tumor growth, cell proliferation, and migration, promoted apoptosis of DLBCL, and inhibited angiogenesis by down-regulating PAR-1-VEGF. RH inhibits proliferation, migration, and angiogenesis of DLBCL cells by down-regulating PAR-1-VEGF.

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 termsHumansHirudinsReceptor, PAR-1Lymphoma, Large B-Cell, DiffuseAnimalsVascular Endothelial Growth Factor AMiceCell Line, TumorNeovascularization, PathologicApoptosisRecombinant ProteinsCell Proliferation

Summary

Hirudin is one of the specific inhibitors of thrombin, which has been confirmed to have strong bioactivities, including inhibiting tumors.

Why This Matters for Hirudotherapy

This study investigated recombinant hirudin (RH), described as one of the specific inhibitors of thrombin, for its effects on diffuse large B-cell lymphoma (DLBCL) using cell lines and mouse models. RH inhibited tumor growth, cell proliferation, migration, and angiogenesis while promoting apoptosis, with the mechanism involving down-regulation of the PAR-1–VEGF signaling axis. This is relevant to ASH's domain as it explores therapeutic effects of hirudin, a thrombin inhibitor, in an oncology context. Caveat: This is a preclinical study using recombinant hirudin (a pharmaceutical product); no leech therapy or leech-derived material is involved, and findings require clinical validation before any therapeutic application.

Citation

Recombinant hirudin suppresses angiogenesis of diffuselarge B-cell lymphoma through regulation of the PAR-1-VEGF

Zhao J et al. · Chemical biology & drug design, 2024

DOI

Added to ASH library: May 27, 2026 · Site last updated: June 18, 2026

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