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Hirudin Regulates Vascular Function in Chronic Renal Failure through Modulating Macrophage Polarization
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-inflammato...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9042600/ https://www.ncbi.nlm.nih.gov/pubmed/35496058 http://dx.doi.org/10.1155/2022/6043698 |
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author | Chen, Bo Ding, Xunfang Yang, Yanbo |
author_facet | Chen, Bo Ding, Xunfang Yang, Yanbo |
author_sort | Chen, Bo |
collection | PubMed |
description | 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-γ), the increased M1/M2 ratio and enhanced levels of inflammatory factors were observed. Furthermore, Hiru boosted the proliferation and ameliorated the inflammatory response and apoptosis of rat VSMCs during the process of coincubation of M1-conditioned medium (CM). Collectively, Hiru played a protective role against vascular injury in CRF directly or through its influence on M1 macrophage polarization and inflammation. |
format | Online Article Text |
id | pubmed-9042600 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-90426002022-04-27 Hirudin Regulates Vascular Function in Chronic Renal Failure through Modulating Macrophage Polarization Chen, Bo Ding, Xunfang Yang, Yanbo Biomed Res Int Research Article 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-γ), the increased M1/M2 ratio and enhanced levels of inflammatory factors were observed. Furthermore, Hiru boosted the proliferation and ameliorated the inflammatory response and apoptosis of rat VSMCs during the process of coincubation of M1-conditioned medium (CM). Collectively, Hiru played a protective role against vascular injury in CRF directly or through its influence on M1 macrophage polarization and inflammation. Hindawi 2022-04-19 /pmc/articles/PMC9042600/ /pubmed/35496058 http://dx.doi.org/10.1155/2022/6043698 Text en Copyright © 2022 Bo Chen et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Chen, Bo Ding, Xunfang Yang, Yanbo Hirudin Regulates Vascular Function in Chronic Renal Failure through Modulating Macrophage Polarization |
title | Hirudin Regulates Vascular Function in Chronic Renal Failure through Modulating Macrophage Polarization |
title_full | Hirudin Regulates Vascular Function in Chronic Renal Failure through Modulating Macrophage Polarization |
title_fullStr | Hirudin Regulates Vascular Function in Chronic Renal Failure through Modulating Macrophage Polarization |
title_full_unstemmed | Hirudin Regulates Vascular Function in Chronic Renal Failure through Modulating Macrophage Polarization |
title_short | Hirudin Regulates Vascular Function in Chronic Renal Failure through Modulating Macrophage Polarization |
title_sort | hirudin regulates vascular function in chronic renal failure through modulating macrophage polarization |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9042600/ https://www.ncbi.nlm.nih.gov/pubmed/35496058 http://dx.doi.org/10.1155/2022/6043698 |
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