ArticleInternational journal of molecular medicine2018
Baicalin inhibits PDGF-BB-induced hepatic stellate cell proliferation, apoptosis, invasion, migration and activation via the miR-3595/ACSL4 axis.
Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 73 citations in OpenAlex.
- ACSL4 in Alzheimer's disease: Pathogenetic mechanisms and potential therapeutic targets.Genes & diseases · 2026Review
- Chemoproteomics identifies STAT3 as a key target of baicalin in ameliorating liver fibrosis.National science review · 2026Article
- Acyl-CoA Synthetase Long-Chain Family Member 4 in Liver Injury: Multidimensional Regulation and Therapeutic Potential.Gastroenterology research · 2026Review
- Immune System and Hepatic Stellate Cells' Crosstalk in Liver Fibrosis: Pathways and Therapeutic Potential.Journal of immunology research · 2026Review
- Exploring ferroptosis and miRNAs: implications for cancer modulation and therapy.Molecular and cellular biochemistry · 2025Review
- ACSL3 is a promising therapeutic target for alleviating anxiety and depression in Alzheimer's disease.GeroScience · 2025Article
- Preventive and Therapeutic Effects of Baicalein, Galangin, and Isorhamnetin in Chronic Liver Diseases: A Narrative Review.Molecules (Basel, Switzerland) · 2025Review
- Advancements in Plant-Based Therapeutics for Hepatic Fibrosis: Molecular Mechanisms and Nanoparticulate Drug Delivery Systems.International journal of molecular sciences · 2024Review
- Noncoding RNA-Mediated Epigenetic Regulation in Hepatic Stellate Cells of Liver Fibrosis.Non-coding RNA · 2024Review
- Chondroprotective effects of bone marrow mesenchymal stem cell-derived exosomes in osteoarthritis.Journal of bioenergetics and biomembranes · 2024Article
- Mechanism and Progress of Natural Products in the Treatment of NAFLD-Related Fibrosis.Molecules (Basel, Switzerland) · 2023Review
- Recent Updates on Viral Oncogenesis: Available Preventive and Therapeutic Entities.Molecular pharmaceutics · 2023Review
- Review
- ACSL4-Mediated Ferroptosis and Its Potential Role in Central Nervous System Diseases and Injuries.International journal of molecular sciences · 2023Review
- Deciphering the Mechanism of Wogonin, a Natural Flavonoid, on the Proliferation of Pulmonary Arterial Smooth Muscle Cells by Integrating Network Pharmacology and In Vitro Validation.Current issues in molecular biology · 2023Article
- Role of baicalin as a potential therapeutic agent in hepatobiliary and gastrointestinal disorders: A review.World journal of gastroenterology · 2022Review
- Regulatory pathways and drugs associated with ferroptosis in tumors.Cell death & disease · 2022Review
- Long non-coding RNA-non-coding RNA activated by DNA damage inhibition suppresses hepatic stellate cell activation via microRNA-495-3p/sphingosine 1-phosphate receptor 3 axis.Bioengineered · 2022Article
- MACC1 regulates the AKT/STAT3 signaling pathway to induce migration, invasion, cancer stemness, and suppress apoptosis in cervical cancer cells.Bioengineered · 2022Article
- Kinsenoside Protects Against Radiation-Induced Liver FibrosisFrontiers in pharmacology · 2022Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatic fibrosis is a physiological response to liver injury that includes a range of cell types. The pathogenesis of hepatic fibrosis currently focuses on hepatic stellate cell (HSC) activation into muscle fiber cells and fibroblasts. Baicalin is a flavone glycoside. It is the glucuronide of baicalein, which is extracted from the dried roots of Scutellaria baicalensis Georgi. Previous work focused on the anti‑viral, ‑inflammatory and ‑tumor properties of baicalin. However, the potential anti‑fibrotic effects and mechanisms of baicalin are not known. The present study demonstrated that baicalin influenced the activation, proliferation, apoptosis, invasion and migration of platelet‑derived growth factor‑BB‑induced activated HSC‑T6 cells in a dose‑dependent manner. To investigate the anti‑fibrotic effect of baicalin, a one‑color micro (mi)RNA array and reverse transcription‑quantitative polymerase chain reaction analyses were used. Results demonstrated that baicalin increased the expression of the miRNA, miR‑3595. In addition, the inhibition of miR‑3595 substantially reversed the anti‑fibrotic effect of baicalin. The present data also suggested that miR‑3595 negatively regulates the long‑chain‑fatty‑acid‑CoA ligase 4 (ACSL4). Furthermore, ACSL4 acted in a baicalin‑dependent manner to exhibit anti‑fibrotic effects. Taken together, it was concluded that baicalin induces miR‑3595 expression that modulates the expression levels of ACSL4. To the best of our knowledge, the present study is the first to demonstrate that baicalin induces overexpression of human miR‑3595, and subsequently decreases the expression of ACSL4, resulting in an anti-fibrotic effect.
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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.