ArticleDrug design, development and therapy2025
Ursolic Acid Ameliorates Diabetic Nephropathy by Inhibiting JAK2/STAT3-Driven Ferroptosis: Mechanistic Insights from Network Pharmacology and Experimental Validation.
Article in Drug design, development and therapy, 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.
- Programmed cell death in kidney disease: integrated crosstalk among ferroptosis, pyroptosis, apoptosis, and cuproptosis.Apoptosis : an international journal on programmed cell death · 2026Review
- Ononin combined withBiochemistry and biophysics reports · 2026Article
- Decursin ameliorates diabetic kidney disease by attenuating renal epithelial-mesenchymal transition via inhibition of the PI3K/Akt pathway.American journal of translational research · 2026Article
- Current Research on the Control Mechanisms of Cell Survival and Proliferation as Potential Interaction Sites with Pentacyclic Triterpenoids in Ovarian Cancer.International journal of molecular sciences · 2025Review
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Authors and funding
6 authors.
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Abstract
Purpose: Ursolic acid (UA) improves diabetic nephropathy (DN), but its regulatory mechanism requires further verification. Methods: The bioactive component-target network of UA in DN was determined using a network pharmacology approach. DN mice (STZ-diabetic C57BL/6 mice, n = 8/group, 4 weeks) were treated with UA (25 mg/kg and 100 mg/kg) and the JAK agonist RO8191 (2 mg/kg). The DN cell model (high glucose-injured NRK-52E cells) was treated with UA (10 and 50 µM) and RO8191 (2 μM) for 24 h. The molecular mechanisms by which UA acts were further verified in vivo and in vitro. Results: UA treatment ameliorated the general state of the DN mouse model, as characterized by the attenuation of weight loss and downregulation of fasting blood glucose (FBG) and fasting serum insulin (FINS) levels (all Conclusion: UA protected against DN by blocking JAK2/STAT3-mediated ferroptosis.
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