ArticleFrontiers in nutrition2025
Curcumin attenuates liver injury by modulating the AGE-RAGE axis and metabolic homeostasis in high-fat diet/streptozotocin-induced type 2 diabetic mice.
Article in Frontiers in nutrition, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Broccoli Sprout Extract Restores Renal Lipid Metabolism in High-Fat Diet-Fed Mice Involving Modulation of AMPK/Nrf2 Signaling and the NLRP3 Inflammasome.Food science & nutrition · 2026Article
- Curcumin ameliorates fatty liver hemorrhagic syndrome in broiler breeders by regulating lipid metabolism via the gut-liver axis.Poultry science · 2026Article
- The Use of Curcumin to Target Oxidative Stress and Inflammation in Type 2 Diabetes Mellitus and Its Complications: Molecular Mechanisms and Therapeutic Perspectives.Antioxidants (Basel, Switzerland) · 2026Review
- Exploration of the Potential Mechanisms of Anaphalis virgata Extract in Treating Diabetic Hepatic Injury Based on Network Pharmacology and Experimental Validation.Chemistry & biodiversity · 2026Article
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Authors and funding
11 authors.
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Abstract
Background: Diabetic liver injury is a serious complication of type 2 diabetes mellitus (T2DM). Curcumin (CUR), a natural polyphenol derived from Methods: We integrated network pharmacology to identify common targets between CUR and T2DM, followed by molecular docking to evaluate binding affinities to key targets. Results: Network pharmacology revealed 256 overlapping targets between CUR and T2DM. Protein-protein interaction (PPI) analysis identified AKT1, TNF, TP53, IL-6, and EGFR as central hub targets. KEGG pathway enrichment suggested the involvement of the advanced glycation end products (AGE)-RAGE signaling pathway in the protective effects of CUR. Molecular docking demonstrated strong binding affinities of CUR with RAGE, AKT1, and TP53. Conclusion: CUR protects against diabetic liver injury by inhibiting AGE-RAGE-induced inflammation and metabolic dysregulation. The protective mechanism involves modulation of the AGE-RAGE axis and restoration of metabolic homeostasis.
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