ArticleMolecular medicine (Cambridge, Mass.)2023
Indole-3-propionic acid alleviates chondrocytes inflammation and osteoarthritis via the AhR/NF-κB axis.
Article in Molecular medicine (Cambridge, Mass.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
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Who cites it
75 citing papers in PubMed, 103 citations in OpenAlex.
- Engineered probiotic-derived indole-3-propionic acid inhibits ubiquitination via AHR signaling to treat postmenopausal osteoporosis.Gut microbes · 2026Article
- ROS-responsive hydrogel delivering liposomal indole-3-propionic acid promotes spinal cord injury repair by enhancing CX3CL1-CX3CR1 mediated neuron-microglia communication.Materials today. Bio · 2026Article
- Metabolic shifts driven by host-microbial interactions.The FEBS journal · 2026Review
- The Microbiota Metabolite-Joint Axis: Mechanistic Insights and Therapeutic Targets for Osteoarthritis.Biomedicines · 2026Review
- Dietary Tryptophan Supplementation Attenuates Lipopolysaccharide-Induced Acute Lung Injury in a Murine Model of Colitis.Nutrients · 2026Article
- Eggshell Membrane Peptides Alleviate IL-1β-Induced Inflammatory Responses and Extracellular Matrix Degradation in Canine Chondrocytes by Inhibiting the NF-κB Signaling Pathway.Animals : an open access journal from MDPI · 2026Article
- Strontium ameliorates tibial dyschondroplasia in broilers through gut microbiota-mediated retinoic acid metabolism.NPJ biofilms and microbiomes · 2026Article
- Effects and mechanisms of synovial mesenchymal stem cell-derived extracellular vesicular LncRNA-SNHG14 on chondrocyte injury.Regenerative therapy · 2026Article
- The gut-joint axis in osteoarthritis.Nature reviews. Rheumatology · 2026Review
- Dysregulation of the glycolysis-mitochondrial metabolism axis in osteoarthritis: mechanisms and therapeutic implications.Journal of orthopaedic translation · 2026Review
- Plant-derived indole alkaloids in chronic inflammatory diseases: molecular mechanisms, therapeutic potential and translational challenges.Inflammopharmacology · 2026Review
- Research advances on Cordyceps sinensis and its components in relation to omics biomarkers for the neurological disorders.Die Naturwissenschaften · 2026Review
- Review
- Ectodysplasin-A (EDA) Signaling Cross-Talk in Skeletogenesis.Calcified tissue international · 2026Review
- Asiaticoside protects against PDF-induced peritoneal fibrosis via suppression of AhR/Nrf2-mediated MMT and oxidative stress.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Advances in the mechanisms of the NLRP3 inflammasome in sepsis‑induced cardiomyopathy and targeted therapeutic studies (Review).Molecular medicine reports · 2026Review
- Propionate-engineered probiotics reduce radiation-induced intestinal damage.Bioresources and bioprocessing · 2026Article
- Gout Inflammation Time Programming: Molecular Clock from Crystal Triggering to Tissue Remodeling.International journal of molecular sciences · 2026Review
- PRKACB Attenuates Chondrocyte Loss and Inflammation in Osteoarthritis.Immunity, inflammation and disease · 2026Article
- Gut and Joint Microbiome and Dysbiosis: A New Perspective on the Pathogenesis and Treatment of Osteoarthritis.Pathogens (Basel, Switzerland) · 2026Review
15 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOsteoarthritis (OA) is a common chronic disease characterized by chronic inflammation and extracellular matrix degradation. Indole-3-propionic acid (IPA) is a tryptophan metabolite secreted by intestinal flora, which can exert anti-inflammatory effects in a variety of diseases. In this study, we further investigated the potential therapeutic role of IPA in OA and the underlying mechanism.
methodsIL-1β was utilized to induce chondrocyte inflammation. Then, the cytotoxicity of IPA on rat chondrocytes was assessed. Meanwhile, RT-qPCR, Griess reaction, ELISA, Western blot and immunofluorescence were performed to evaluate the expression of inflammatory factors and stromal proteins, and the NF-κB pathway in chondrocytes treated with IL-1β alone, with IPA or with aryl hydrocarbon receptor (AhR) knockdown. An OA rat model was established by anterior cruciate ligament transection, and hematoxylin-eosin staining, Safranin-O/Fast Green staining and immunochemistry were applied to estimate OA severity.
resultsIPA did not affect cellular viability at concentrations up to 80 µM. IPA significantly inhibited the IL-1β-induced expression of inflammatory factors (Nitric oxide, PGE2, TNF-α, IL-6, iNOS and COX-2) and matrix-degrading enzymes (MMP-3, MMP-13 and ADAMTS-5), upregulated the expression of anabolic markers (aggrecan and collagen-II) and inactivated the NF-κB pathway. However, AhR knockdown could abolish the above protection capabilities and the suppression of the NF-κB pathway induced by IPA. Furthermore, IPA significantly reduced serum inflammatory cytokines expression, cartilage destruction and synovitis in vivo, demonstrating its protective role in OA progression.
conclusionIPA improved IL-1β-induced chondrocyte inflammation and extracellular matrix degradation through the AhR/NF-κB axis, which provides an innovative therapeutic strategy for OA.
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