ArticleHeliyon2024
Hirudin inhibit the formation of NLRP3 inflammasome in cardiomyocytes via suppressing oxidative stress and activating mitophagy.
Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Unveiling a novel pathway: Ginseng vanillic acid fights heart failure by coupling mitophagy to pyroptosis through the PINK1-BRCA1-NLRP3 axis.Journal of ginseng research · 2026Article
- Protective Effect of the NHE1 Inhibitor Buthutin A on Oxidative Stress-Induced Apoptosis in HUVECs.ACS omega · 2026Article
- The Advances in Novel Delivery Strategies for Hirudin Against Cardiovascular Diseases.Pharmaceuticals (Basel, Switzerland) · 2026Review
- A Brief Description of the Cellular Mechanisms Involved in Cardiac Chemical Hypoxia.Cardiovascular toxicology · 2026Review
- Mitophagy-pyroptosis-macrophage polarization crosstalk in cardiovascular diseases: mechanistic insights and therapeutic potential.Frontiers in cardiovascular medicine · 2026Review
- A Biomimetic Macrophage-Membrane-Fused Liposomal System Loaded with GVs-HV Recombinant Plasmid for Targeted Anti-Atherosclerosis Therapy.Pharmaceutics · 2025Article
- Stepwise targeting hyaluronic acid-based polymeric prodrug for acute kidney injury and prevents its progression to chronic kidney disease.Materials today. Bio · 2025Article
- Mitochondrial DNA Dysfunction in Cardiovascular Diseases: A Novel Therapeutic Target.Antioxidants (Basel, Switzerland) · 2025Review
- Hirudin Alleviates Early Brain Injury After Subarachnoid Hemorrhage in Rats via Regulating NLRP3 Inflammasome-Mediated Pyroptosis.Physiological research · 2025Article
- Electroacupuncture Regulates Oxidative Stress-Mediated NLRP3/ASC/Caspase-1 Pathway to Inhibit Microglial Activation: Alleviating Neuroinflammation and Depression in IBD.Journal of inflammation research · 2025Article
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Context: Cardiomyocyte hypertrophy due to hemodynamic overload eventually leads to heart failure. Hirudin has been widely used in the treatment of cardiovascular diseases and NLRP3 inflammasome was proven to induce cardiomyocyte pyroptosis. However, the mechanism by which it inhibits cardiomyocyte hypertrophy remains unclear. Objective: To explore the mechanism of hirudin inhibiting cardiomyocyte hypertrophy based on NLRP3 inflammasome activation and mitophagy. Materials & methods: 1 μM AngII was used for cardiac hypertrophy modeling in H9C2 cells, and cell viability was quantified by CCK-8 assay to screen the appropriate action concentrations of hirudin. After that, we cultured AngII induced-H9C2 cells for 24 h with 0, 0.3, 0.6, and 1.2 mM hirudin, respectively. Next, we marked H9C2 cells with phalloidine and observed them using fluorescence microscope. IL-1β, IL-18, IL-6, TNF-α, ANP, BNP, β-MHC, and mtDNA were analyzed by qRT-PCR; ROS were quantified by Flow cytometry; SOD, MDA, and GSH-Px were detected by ELISA; and proteins including NLRP3, ASC, caspase-1, pro-caspase-1, IL-1β, IL-18, PINK-1, Parkin, beclin-1, LC3-Ⅰ, LC3-Ⅱ, p62, were quantified by western blotting. Results: It was discovered that hirudin reduced the superficial area of AngII-induced H9C2 cells and inhibited the AngII-induced up-regulation of ANP, BNP, and β-MHC. Besides, hirudin down-regulated the expressions of NLRP3 inflammasome-related cytokines, containing IL-1β, IL-18, IL-6, TNF-α. It also down-regulated the expression of mtDNA and ROS, decreased the expression levels of NLRP3 inflammasome activation related proteins, including NLRP3, ASC, caspase-1, pro-caspase-1, IL-1β, IL-18; and increased the expressions of PINK-1, Parkin, beclin-1, LC3-Ⅱ/LC3-Ⅰ, p62 in AngII-induced H9C2 cells. Discussion: Hirudin promoted the process of mitophagy, inhibited the development of inflammation and oxidative stress, and inhibited the activation of the NLRP3 inflammasome and the PINK-1/Parkin pathway. Conclusion: Hirudin has the activity to suppress cardiac hypertrophy may benefit from the inhibition of NLRP3 inflammasome and activating of PINK-1/Parkin related-mitophagy.
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