ArticleBioMed research international2022
Hirudin Regulates Vascular Function in Chronic Renal Failure through Modulating Macrophage Polarization.
Article in BioMed research international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- A network pharmacology-based study on the mechanism of hirudin attenuates renal interstitial fibrosis through Nrf2 and NF-κB signalling pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Molecular Insights into Leech-Derived Bioactive Compounds: Biochemical Mechanisms and Therapeutic Potential.International journal of molecular sciences · 2026Review
- Tumor-Associated Macrophages as Key Modulators of Disease Progression in Diffuse Large B-Cell Lymphoma.Biomedicines · 2025Review
- Hirudin inhibits ferroptosis to improve renal fibrosis by targeting the STAT3/NLRP3 signaling pathway.Acta cirurgica brasileira · 2025Article
- The Pathological Mechanisms and Therapeutic Molecular Targets in Arteriovenous Fistula Dysfunction.International journal of molecular sciences · 2024Review
- Recombinant hirudin and PAR-1 regulate macrophage polarisation status in diffuse large B-cell lymphoma.BMC biotechnology · 2024Article
- Hirudin in the Treatment of Chronic Kidney Disease.Molecules (Basel, Switzerland) · 2024Review
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excessive inflammation is responsible for arteriovenous fistula (AVF) failure, which determines the therapeutic effect of chronic renal failure (CRF). Macrophage polarization is of great significance in the inflammatory response. Hirudin (Hiru) has been reported to possess a definite anti-inflammatory effect. This study is to uncover the impacts of Hiru on classically (M1)/alternatively (M2) macrophage polarization in the CRF rat model and rat vascular smooth muscle cells (VSMCs). After the CRF rat model was administrated with different concentrations of Hiru, blood urea nitrogen (BUN) and serum creatinine (Scr) levels were tested. H&E staining was to detect vascular injury, and IHC assay was to analyze inducible nitric oxide synthase (iNOS) and arginase-1 (Arg-1) expressions in vascular tissues. Levels of inflammatory factors were examined by ELISA. Besides, western blot was to estimate the levels of marker proteins related to macrophage, proliferation, and apoptosis. CCK-8 was to measure cell viability. We discovered that Hiru alleviated renal function injury and vascular injury, exacerbated VSMC hyperplasia, and stimulated the differentiation and activation of M1 macrophage towards M2 macrophage in vivo. Moreover, after treatment with lipopolysaccharide (LPS)/IFN-gamma (IFN-
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