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Phenotypic Characterization of Macrophages from Rat Kidney by Flow Cytometry
Published on: October 18, 2016
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Hirudin Regulates Vascular Function in Chronic Renal Failure through Modulating Macrophage Polarization
Bo Chen1, Xunfang Ding1, Yanbo Yang1
1Department of Nephrology, Lianyungang Hospital of Traditional Chinese Medicine, Lianyungang, Jiangsu 222000, China.
Biomed Research International
|May 2, 2022
Summary
Hirudin (Hiru) alleviates vascular injury in chronic renal failure (CRF) by shifting M1 macrophages to M2, reducing inflammation and improving kidney function in rats.
Area of Science:
- Vascular Biology
- Immunology
- Nephrology
Background:
- Arteriovenous fistula (AVF) failure in chronic renal failure (CRF) is linked to excessive inflammation.
- Macrophage polarization (M1/M2) plays a critical role in regulating inflammatory responses.
- Hirudin (Hiru) exhibits known anti-inflammatory properties.
Purpose of the Study:
- To investigate the effects of Hirudin on macrophage polarization (M1/M2) in a CRF rat model.
- To evaluate Hirudin's impact on vascular smooth muscle cells (VSMCs) and inflammatory markers in CRF.
Main Methods:
- CRF rat model administration with varying Hirudin concentrations.
- Biochemical assays (BUN, Scr), histological staining (H&E), immunohistochemistry (iNOS, Arg-1), ELISA for inflammatory factors.
- Western blot for protein markers, CCK-8 assay for cell viability.
Main Results:
- Hirudin improved renal function and reduced vascular injury in CRF rats.
- Hirudin promoted M1 to M2 macrophage polarization and decreased inflammatory factors.
- Hirudin enhanced VSMC proliferation and reduced inflammation and apoptosis in M1-conditioned medium.
Conclusions:
- Hirudin offers a protective effect against vascular injury in CRF.
- This protection is mediated partly by modulating M1 macrophage polarization and inflammation.
- Hirudin demonstrates therapeutic potential for managing vascular complications in CRF.
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