ArticleBritish journal of pharmacology2013
3,3'-Diindolylmethane ameliorates experimental hepatic fibrosis via inhibiting miR-21 expression.
Article in British journal of pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 38 citations in OpenAlex.
- Aryl hydrocarbon receptor: a multifaceted environmental sensor in liver homeostasis and disease.Frontiers in medicine · 2026Review
- Unveiling the Multifaceted Pharmacological Actions of Indole-3-Carbinol and Diindolylmethane: A Comprehensive Review.Plants (Basel, Switzerland) · 2025Review
- The aryl hydrocarbon receptor in liver injury: a double-edged sword in roles, mechanisms, and future perspectives.Frontiers in pharmacology · 2025Review
- 3,3'-Diindolylmethane improves antitumor immune responses of PD-1 blockade via inhibiting myeloid-derived suppressor cells.Chinese medicine · 2022Article
- N-n-Butyl haloperidol iodide ameliorates liver fibrosis and hepatic stellate cell activation in mice.Acta pharmacologica Sinica · 2022Article
- The aryl hydrocarbon receptor in liver inflammation.Seminars in immunopathology · 2021Review
- Glucobrassicin Metabolites Ameliorate the Development of Portal Hypertension and Cirrhosis in Bile Duct-Ligated Rats.International journal of molecular sciences · 2019Article
- MiR-21b-3p protects NS2OY cells against oxygen-glucose deprivation/reperfusion-induced injury by down-regulating cyclooxygenase-2.American journal of translational research · 2019Article
- 3,3'-Diindolylmethane ameliorates renal fibrosis through the inhibition of renal fibroblast activation in vivo and in vitro.Renal failure · 2018Article
- Knockout of microRNA-21 reduces biliary hyperplasia and liver fibrosis in cholestatic bile duct ligated mice.Laboratory investigation; a journal of technical methods and pathology · 2016Article
- Hepatic Stellate Cells and microRNAs in Pathogenesis of Liver Fibrosis.Journal of clinical medicine · 2016Review
- Micro-RNA 21 inhibition of SMAD7 enhances fibrogenesis via leptin-mediated NADPH oxidase in experimental and human nonalcoholic steatohepatitis.American journal of physiology. Gastrointestinal and liver physiology · 2015Article
- The mechanisms of HSC activation and epigenetic regulation of HSCs phenotypes.Current pathobiology reports · 2014Article
- Pathogenesis of liver cirrhosis.World journal of gastroenterology · 2014Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeHepatic fibrosis is a type of liver disease characterized by excessive collagen deposition produced by activated hepatic stellate cells (HSCs), and no appropriate drug treatment is available clinically. The microRNA, miR-21 exhibits an important role in the pathogenesis and progression of hepatic fibrosis. 3,3'-Diindolylmethane (DIM) is a natural autolytic product in plants and can down-regulate miR-21 expression. Here we have assessed the therapeutic effects of DIM against hepatic fibrosis and investigated the underlying mechanisms. EXPERIMENTAL APPROACH: The effects of DIM on HSC activation were measured by analysing the expression of α-smooth muscle actin and collagen I in both HSC-T6 cell line and primary HSCs. Expression of miR-21 was also measured after DIM treatment and the therapeutic effect of DIM was further studied in vivo, using the model of hepatic fibrosis induced by thioacetamide in mice. The antagonist oligonucleotide, antagomir-21, was also used to suppress the effects of miR-21. KEY
resultsDIM suppressed the central TGF-β signalling pathway underlying HSC activation by down-regulating the expression of miR-21. The decreased miR-21 expression was achieved by inhibiting the activity of the transcription factor, AP-1. Moreover, DIM blunted the activation phenotype of primary HSCs. Administration of DIM in vivo attenuated liver fibrosis induced by thioacetamide, as assessed by collagen deposition and profiles of profibrogenic markers. CONCLUSIONS AND IMPLICATIONS: DIM shows potential as a therapeutic agent for the treatment of hepatic fibrosis.
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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.