ArticleMedical science monitor : international medical journal of experimental and clinical research2018
Hirudin Protects Ang II-Induced Myocardial Fibroblasts Fibrosis by Inhibiting the Extracellular Signal-Regulated Kinase1/2 (ERK1/2) Pathway.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- The Advances in Novel Delivery Strategies for Hirudin Against Cardiovascular Diseases.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Exosomal miR-15a-5p from cardiomyocytes promotes myocardial fibrosis.Molecular and cellular biochemistry · 2025Article
- Distribution and Blood Penetration of Hirudin in Various Organs and Tissues of Rabbits With Carotid Artery Injury by Ultraperformance Liquid Chromatography-Tandem Mass Spectrometry.Journal of analytical methods in chemistry · 2025Article
- Recombinant hirudin attenuates pulmonary hypertension and thrombosis in acute pulmonary embolism rat model.PeerJ · 2024Article
- Hirudin ameliorates myocardial ischemia-reperfusion injury in a rat model of hemorrhagic shock and resuscitation: roles of NLRP3-signaling pathway.Molecular and cellular biochemistry · 2024Article
- Peptides fromACS omega · 2023Article
- Network Pharmacology andFrontiers in pharmacology · 2022Article
- Pharmacological Activities and Mechanisms of Hirudin and Its Derivatives - A Review.Frontiers in pharmacology · 2021Review
- Huayu Tongluo Recipe Attenuates Renal Oxidative Stress and Inflammation through the Activation of AMPK/Nrf2 Signaling Pathway in Streptozotocin- (STZ-) Induced Diabetic Rats.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Roles of Biomarkers in Myocardial Fibrosis.Aging and disease · 2020Review
- Hirudin Reduces the Expression of Markers of the Extracellular Matrix in Renal Tubular Epithelial Cells in a Rat Model of Diabetic Kidney Disease Through the Hypoxia-Inducible Factor-1α (HIF-1α)/Vascular Endothelial Growth Factor (VEGF) Signaling Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Hirudin Ameliorates Renal Interstitial Fibrosis via Regulating TGF-Evidence-based complementary and alternative medicine : eCAM · 2020Article
- The Association of Ascorbic Acid, Deferoxamine and N-Acetylcysteine Improves Cardiac Fibroblast Viability and Cellular Function Associated with Tissue Repair Damaged by Simulated Ischemia/Reperfusion.Antioxidants (Basel, Switzerland) · 2019Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND Myocardial fibrosis is closely related to all types of cardiovascular diseases. Hirudin is widely used in the prevention and treatment of cardiovascular diseases and cancers. In this study, we examined the potential role(s) and mechanism of hirudin in angiotensin II (Ang II)-induced myocardial fibrosis. MATERIAL AND METHODS The viability of myocardial fibroblasts, and reactive oxygen species (ROS) rates were measured respectively using cell counting kit-8 (CCK-8) and flow cytometry. Malondialdehyde (MDA) content, the activities of lactate dehydrogenase (LDH), and superoxide dismutase (SOD) were detected by the respective kits. The mRNA and protein levels of fibrosis-related factors were separately assessed by qRT-PCR and western blot. RESULTS Our data revealed that hirudin suppressed the viability of myocardial fibroblasts, and that it relieved the proliferation induced by Ang II in a dose-dependent manner. We also found that hirudin reduced ROS production, LDH activity, and MDA content; however, it enhanced SOD activity. Moreover, while hirudin significantly downregulated the levels of matrix metalloproteinase-2 (MMP-2), MMP-9, fibronectin (FN), transforming growth factor beta 1 (TGF-β1), collagen-I (COL-I), and COL-III, it upregulated the expression level of tissue inhibitor of metalloproteinases-2 (TIMP-2). Furthermore, phosphorylated extracellular signal-regulated kinase1/2 (p-ERK1/2) was decreased by hirudin, compared to the Ang-II group. CONCLUSIONS Hirudin depressed Ang II-induced myocardial fibroblasts via inhibiting oxidative stress, regulating fibrosis-related factors, and repressing the ERK1/2 pathway.
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Registered trials
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