ArticleInflammopharmacology2023
A low dose of naloxone mitigates autoimmune hepatitis by regulating TLR4/NF-κB and Nrf2/HO-1 signaling pathways.
Article in Inflammopharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Effects of perioperative low-dose naloxone on the immune system in patients undergoing laparoscopic-assisted total gastrectomy: a randomized controlled trial.BMC anesthesiology · 2024Trial
- Structure-guided design and synthesis of Etoricoxib analogues for selective COX-2 inhibition: in vitro assessment and computational insights with prospective in vivo confirmation.Molecular diversity · 2026Article
- Article
- Inhibition of TLR4/TRAF6/NF-κB pathway by empagliflozin mitigates concanavalin A-induced autoimmune hepatitis in mice.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Therapeutic Repurposing of Avanafil Against Lipopolysaccharide-induced Depression and Autoimmune Hepatitis: Gut-brain-liver Axis Orchestration Via Regulation of TLR4/NF-κB/IDO and Nrf2/HO-1 Pathways.Molecular neurobiology · 2026Article
- Next-Generation Dietary Antioxidants in Women's Reproductive Health: Mechanisms, Reproductive Outcomes, and Therapeutic Potential.Antioxidants (Basel, Switzerland) · 2026Review
- Gut microbiota dysbiosis and hepatic inflammation in morphine dependence and withdrawal: insights from a rat model.BMC gastroenterology · 2026Article
- From nutrition to therapeutics: the diverse inflammopharmacological and biomedical roles of astaxanthin.Inflammopharmacology · 2026Review
- Revealing the pathogenesis of autoimmune hepatitis and research progress in drug discovery from hepatic immune cells and intercellular communication signaling mechanisms.Frontiers in immunology · 2026Review
- MiR-122-5p modulates ferroptosis via SLC7A11: A potential therapeutic target in autoimmune hepatitis.Journal of translational autoimmunity · 2025Article
- Health position paper and redox perspectives - Bench to bedside transition for pharmacological regulation of NRF2 in noncommunicable diseases.Redox biology · 2025Review
- HPLC-HRMS/MS and anti-inflammatory effects of bunya pine resin through multifaceted pathway modulation: NUMB/NOTCH1/HES1/mTOR/ PI3K/HMGB1 signaling cascades.Inflammopharmacology · 2025Article
- TRIF-dependent signaling and its role in liver diseases.Frontiers in cell and developmental biology · 2024Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Naloxone is a non-selective opiate receptor antagonist that is mainly used in the management of acute opioid overdose or intoxication. Previously, naloxone has been shown to have anti-inflammatory and antioxidant properties. Concanavalin A (Con A) model is a common and well established animal model of autoimmune hepatitis that closely resembles the pathological alterations that occur in human. The present study demonstrates that a low dose of naloxone (LD NX) has the ability to improve hepatic function and attenuate hepatic damage induced by Con A as indicated by a clear reduction in serum aminotransferase, bilirubin and enhancement of albumin production as well as liver pathological changes. Also, The proinflammatory cytokines, tumor necrosis factor-α (TNF-α), interferon- γ (IFN-γ), interleukin-6 (IL-6) and interleukin-1β (IL-1β) were highly suppressed in animals pretreated with LD NX via interference with TLR4/NF-κB as well as JNK signaling pathways. Furthermore, oxidative stress was highly attenuated in animals pretreated with LD NX as indicated by high reduction in hepatic MDA and an increase in Nrf2, HO-1 expression and subsequent production of the endogenous antioxidants, SOD, CAT and GSH. Collectively, this study demonstrates that LD NX has the ability to mitigate Con A-induced autoimmune hepatitis via modulation of inflammatory cytokines secretion and interference with reactive oxygen species generation.
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