ArticleMolecular biology reports2020
The protective effect of uric acid in reducing TLR4/NF-κB activation through the inhibition of HMGB1 acetylation in a model of ischemia-reperfusion injury in vitro.
Article in Molecular biology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Potential association between magnesium depletion score and hyperuricemia in American adults, a cross-sectional study based on NHANES 2003-2018.Preventive medicine reports · 2025Article
- Hyperuricemia and its related diseases: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2024Review
- Dl-3-n-Butylphthalide (NBP) Mitigates Muscular Injury Induced by Limb Ischemia/Reperfusion in Mice through the HMGB1/TLR4/NF-Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Self-extracellular RNA promotes pro-inflammatory response of astrocytes to exogenous and endogenous danger signals.Journal of neuroinflammation · 2021Article
- Uric Acid as a Predictor for Early Allograft Dysfunction after Living Donor Liver Transplantation: A Prospective Observational Study.Journal of clinical medicine · 2021Article
- Hyperuricemia in Psoriatic Arthritis: Epidemiology, Pathophysiology, and Clinical Implications.Frontiers in medicine · 2021Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Inflammation plays an important role in ischemia-reperfusion injury. Through its antioxidative effects, uric acid can reduce cell injury. However, its mechanism is unknown. This study investigated the protective mechanism of uric acid in cells during ischemia-reperfusion. We divided hippocampal neurons into six groups: the control, OGD, OGD/R, OGD/R + HMGB1 siRNA, OGD/R + uric acid, and OGD/R + uric acid + HMGB1 groups. The MTT assay was used to evaluate cell viability, while apoptosis was detected by flow cytometry. The expression of HMGB1, TLR4, NF-κB-p65 and phosphorylated NF-κB-p65 was detected by Western blotting. The levels of IL-6, IL-1β and TNF-α in the culture medium were determined by ELISA. The results indicated increased cell viability and decreased apoptosis in the presence of HMGB1 siRNA and uric acid but the opposite findings in the presence of HMGB1 protein after OGD/R. Uric acid and HMGB1 siRNA inhibited HMGB1 acetylation to prevent its transport from the nucleus to the cytoplasm. The expression of HMGB1 downstream proteins (TLR4, NF-κB-p65 and phosphorylated NF-κB-p65) and the levels of inflammatory factors in the presence of HMGB1 siRNA and uric acid was lower than those in the presence of HMGB1 protein after OGD or OGD/R. These data indicated that uric acid may prevent cell injury mainly by inhibiting HMGB1 acetylation to regulate TLR4/NF-κB pathways and reduce the levels of inflammatory factors.
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