ArticleActa cirurgica brasileira2025
Hirudin inhibits ferroptosis to improve renal fibrosis by targeting the STAT3/NLRP3 signaling pathway.
Article in Acta cirurgica brasileira, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Mechanisms of Macrophage Glycolytic Reprogramming and Interventional Effects of Traditional Chinese Medicine on Renal Fibrosis.International journal of general medicine · 2026Review
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5 authors.
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Abstract
purposeTo reveal the role and underlying mechanism of hirudin in renal fibrosis.
methodsThe unilateral ureteral obstruction (UUO) rat model and ferroptosis activator RSL3-induced human kidney proximal tubular epithelial cells (HK-2) were established. Hematoxylin-eosin staining, commercial kits, and immunohistochemistry were used to assess the effect of hirudin on renal function and renal fibrosis. Cell counting kit-8 assay was employed to test cell viability. Ferroptosis indicator levels were detected using commercial kits. The protein levels were examined by Western blot. The STAT3 activator colivelin was introduced to verify the role of the STAT3/NLRP3 signaling pathway in ferroptosis.
resultsHirudin alleviated renal injury and improved renal fibrosis in UUO rats. The cell viability of RSL3-treated HK-2 cells was increased after hirudin treatment. In the model group, GPX4, SLC7A11, and glutathione expression decreased, while malondialdehyde and iron content levels increased, indicating that ferroptosis was activated. Besides, p-STAT3 and NLRP3 protein levels were also upregulated. However, hirudin treatment reversed these changes. When the STAT3 activator colivelin was added, the effect of hirudin was altered.
conclusionHirudin improved renal fibrosis by inhibiting ferroptosis via the STAT3/NLRP3 signaling pathway.
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