ArticleBritish journal of pharmacology2015
3,3'-Diindolylmethane attenuates LPS-mediated acute liver failure by regulating miRNAs to target IRAK4 and suppress Toll-like receptor signalling.
Article in British journal of pharmacology, 2015. 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, 26 citations in OpenAlex.
- Shikonin treatment ameliorates lipopolysaccharide-induced acute liver failure in mice via regulating miR-106/MCL1 and miR-34a/SIRT1/TP53 signaling.Archives of medical science : AMS · 2026Article
- Unveiling the Multifaceted Pharmacological Actions of Indole-3-Carbinol and Diindolylmethane: A Comprehensive Review.Plants (Basel, Switzerland) · 2025Review
- Triad3A involved in the regulation of endotoxin tolerance and mycobactericidal activity through the NFκB-nitric oxide pathway.Immunity, inflammation and disease · 2023Article
- MiR-302a Limits Vascular Inflammation by Suppressing Nuclear Factor-κ B Pathway in Endothelial Cells.Frontiers in cell and developmental biology · 2021Article
- miR-106a Targets Anoctamin 1 (ANO1) to Regulate Lipopolysaccharide (LPS)-Induced Inflammatory Response in Macrophages.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Indole-3-Carbinol Derivative DIM Mitigates Carbon Tetrachloride-Induced Acute Liver Injury in Mice by Inhibiting Inflammatory Response, Apoptosis and Regulating Oxidative Stress.International journal of molecular sciences · 2020Article
- Anti-inflammatory activity of diindolylmethane alleviates Riemerella anatipestifer infection in ducks.PloS one · 2020Article
- 3,3'‑Diindolylmethane mitigates lipopolysaccharide‑induced acute kidney injury in mice by inhibiting NOX‑mediated oxidative stress and the apoptosis of renal tubular epithelial cells.Molecular medicine reports · 2019Article
- 3,3'-Diindolylmethane protects cardiomyocytes from LPS-induced inflammatory response and apoptosis.BMC pharmacology & toxicology · 2018Article
- 3,3'-Diindolylmethane ameliorates renal fibrosis through the inhibition of renal fibroblast activation in vivo and in vitro.Renal failure · 2018Article
- Liver-specific deletion of Eva1a/Tmem166 aggravates acute liver injury by impairing autophagy.Cell death & disease · 2018Article
- Herbal Compound "Jiedu Huayu" Reduces Liver Injury in Rats via Regulation of IL-2, TLR4, and PCNA Expression Levels.Evidence-based complementary and alternative medicine : eCAM · 2017Article
- Cellular and Molecular Mechanisms of 3,3'-Diindolylmethane in Gastrointestinal Cancer.International journal of molecular sciences · 2016Review
- 3,39-Diindolylmethane Ameliorates Staphylococcal Enterotoxin B–Induced Acute Lung Injury through Alterations in the Expression of MicroRNA that Target Apoptosis and Cell-Cycle Arrest in Activated T Cells.The Journal of pharmacology and experimental therapeutics · 2016Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
background and purposeAcute liver failure (ALF) is a severe and potentially lethal clinical syndrome. 3,3'-Diindolylmethane (DIM) is a natural plant-derived compound with anti-cancer activities. Recently, DIM has also been shown to have anti-inflammatory properties. Here, we tested the hypothesis that DIM would suppress endotoxin-induced ALF. EXPERIMENTAL APPROACH: We investigated the therapeutic potential of DIM in a mouse model of D-galactosamine/Lipopolysaccharide (GalN/LPS)-induced ALF. The efficacy of DIM treatment was assessed by survival, liver histopathology, serum levels of alanine transaminase, pro-inflammatory cytokines and number of activated liver macrophages. Effects of DIM on the expression of two miRNAs, 106a and 20b, and their predicted target gene were measured by qRT-PCR and Western blotting. Effects of DIM on the release of TNF-α from RAW264.7 macrophages transfected with mimics of these miRNAs and activated by LPS was assessed by elisa. KEY
resultsDIM treatment protected mice from ALF symptoms and reduced the number of activated liver macrophages. DIM increased expression of miR-106a and miR-20b in liver mononuclear cells and decreased expression of their predicted target gene IL-1 receptor-associated kinase 4 (IRAK4), involved in signalling from Toll-like receptor 4 (TLR4). In vitro transfection of RAW264.7 cells using miRNA mimics of miR-106a and 20b decreased expression of IRAK4 and of TNF-α secretion, following LPS stimulation. CONCLUSIONS AND IMPLICATIONS: DIM attenuated GalN/LPS-induced ALF by regulating the expression of unique miRNAs that target key molecules in the TLR4 inflammatory pathway. DIM may represent a potential novel hepatoprotective agent.
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