ArticleInternational journal of molecular medicine2017
Apamin suppresses biliary fibrosis and activation of hepatic stellate cells.
Article in International journal of molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- Molecular mechanisms behind the inhibitory effects of ginsenoside Rg3 on hepatic fibrosis: a review.Archives of toxicology · 2025Review
- The possible protective effect of luteolin on cardiovascular and hepatic changes in metabolic syndrome rat model.Cell and tissue research · 2025Article
- STAT3 Decoy Oligodeoxynucleotides Suppress Liver Inflammation and Fibrosis in Liver Cancer Cells and a DDC-Induced Liver Injury Mouse Model.Molecules (Basel, Switzerland) · 2024Article
- Harnessing the power of bee venom for therapeutic and regenerative medical applications: an updated review.Frontiers in pharmacology · 2024Review
- Protective Effects of Apamin on Acetaminophen-Induced Hepatotoxicity in Mice.Current issues in molecular biology · 2023Article
- Effects of Apamin on MPPInternational journal of molecular sciences · 2022Article
- Protective Effect ofNutrients · 2022Article
- Article
- Protective Effects of Bee Venom-Derived Phospholipase ABiomedicines · 2021Article
- Antioxidative, Antiapoptotic, and Anti-Inflammatory Effects of Apamin in a Murine Model of Lipopolysaccharide-Induced Acute Kidney Injury.Molecules (Basel, Switzerland) · 2020Article
- Bee Venom: An Updating Review of Its Bioactive Molecules and Its Health Applications.Nutrients · 2020Review
- Review: Pathogenesis of cholestatic liver diseases.World journal of hepatology · 2020Review
- Apamin Suppresses LPS-Induced Neuroinflammatory Responses by Regulating SK Channels and TLR4-Mediated Signaling Pathways.International journal of molecular sciences · 2020Article
- Review
- Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cholestatic liver disease is characterized by the progressive destruction of biliary epithelial cells (BECs) followed by fibrosis, cirrhosis and liver failure. Activated hepatic stellate cells (HSCs) and portal fibroblasts are the major cellular effectors of enhanced collagen deposition in biliary fibrosis. Apamin, an 18 amino acid peptide neurotoxin found in apitoxin (bee venom), is known to block Ca2+-activated K+ channels and prevent carbon tetrachloride-induced liver fibrosis. In the present study, we aimed to ascertain whether apamin inhibits biliary fibrosis and the proliferation of HSCs. Cholestatic liver fibrosis was established in mouse models with 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) feeding. Cellular assays were performed on HSC-T6 cells (rat immortalized HSCs). DDC feeding led to increased hepatic damage and proinflammtory cytokine levels. Notably, apamin treatment resulted in decreased liver injury and proinflammatory cytokine levels. Moreover, apamin suppressed the deposition of collagen, proliferation of BECs and expression of fibrogenic genes in the DDC-fed mice. In HSCs, apamin suppressed activation of HSCs by inhibiting the Smad signaling pathway. These data suggest that apamin may be a potential therapeutic target in cholestatic liver disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.