ArticleFrontiers in pharmacology2022
Inhibition of inflammatory liver injury by the HMGB1-A box through HMGB1/TLR-4/NF-κB signaling in an acute liver failure mouse model.
Article in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- IL‑17AInternational journal of molecular medicine · 2026Article
- Parkin Induces Ubiquitination and Large Extracellular Vesicle Release of HMGB1 to Activate Antitumor Immunity.Cancer research · 2025Article
- Protective effects of melatonin and naringenin against acitretin induced hepatotoxicity via modulation of oxidative stress and inflammatory signaling.Scientific reports · 2025Article
- 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
- Induction of ferroptosis by SIRT1 knockdown alleviates cytarabine resistance in acute myeloid leukemia by activating the HMGB1/ACSL4 pathway.International journal of oncology · 2025Article
- Emerging Roles of High-mobility Group Box-1 in Liver Disease.Journal of clinical and translational hepatology · 2024Review
- Orchestrated regulation of immune inflammation with cell therapy in pediatric acute liver injury.Frontiers in immunology · 2023Review
- Advances in the study of acetaminophen-induced liver injury.Frontiers in pharmacology · 2023Review
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We aimed to investigate the preventive effect of high mobility group box 1 (HMGB1)-A box and the mechanism by which it alleviates inflammatory injury in acute liver failure (ALF) by inhibiting the extracellular release of HMGB1. BALB/c mice were intraperitoneally (i.p.) administered LPS/D-GalN to establish an ALF mouse model. HMGB1-A box was administered (i.p.) 1 h before establishing the ALF mouse model. The levels of extracellularly released HMGB1, TLR-4/NF-κB signaling molecules, the proinflammatory cytokines TNF-α, IL-1β, and IL-6 and COX-2 were measured in the liver tissue and/or serum by Immunohistochemistry, Western blotting and Enzyme-linked immunosorbent assay (ELISA). The levels of extracellularly released HMGB1, TLR-4/NF-κB signaling molecules and proinflammatory cytokines were measured in Huh7 cells as well as LPS- and/or HMGB1-A box treatment by confocal microscopy, Western blotting and ELISA. In the ALF mouse model, the levels of HMGB1 were significantly increased both in the liver and serum, TLR-4/NF-κB signaling molecules and proinflammatory cytokines also was upregulated. Notably, HMGB1-A box could reverse these changes. HMGB1-A box could also cause these changes in LPS-induced Huh7 cells. HMGB1-A box played a protective role by inhibiting inflammatory liver injury
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