ArticleWorld journal of diabetes2024
Asiaticoside improves diabetic nephropathy by reducing inflammation, oxidative stress, and fibrosis: An
Article in World journal of diabetes, 2024. 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.
- Therapeutic potential ofPharmaceutical biology · 2026Review
- PTBP3 promotes diabetic nephropathy via Smad3-dependent podocyte-mesenchymal transition.Molecular biology reports · 2026Article
- Natural Products as Potential Therapeutic Candidates for Diabetic Kidney Disease: Molecular Mechanisms, Translational Challenges, and Future Prospects.International journal of molecular sciences · 2025Review
- D-Psicose mitigates NAFLD mice induced by a high-fat diet by reducing lipid accumulation, inflammation, and oxidative stress.Frontiers in nutrition · 2025Article
- Neuroprotective Effects of Asiatic Acid on Autophagy and Mitochondrial Integrity in a Parkinson's Disease Cellular Model.Journal of experimental pharmacology · 2025Article
- Global research hotspots and trends in oxidative stress-related diabetic nephropathy: a bibliometric study.Frontiers in endocrinology · 2024Article
Corrections and comments
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Authors and funding
6 authors.
Funding
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Abstract
backgroundDiabetic nephropathy (DN) is a severe microvascular complication of diabetes characterized by inflammation, oxidative stress, and renal fibrosis. Asiaticoside (AC) exhibits anti-inflammatory, antioxidant, and anti-fibrotic properties, suggesting potential therapeutic benefits for DN. This study aimed to investigate the protective effects of AC against DN and elucidate the underlying mechanisms involving the nuclear factor erythroid 2-related factor 2 (NRF2)/heme oxygenase-1 (HO-1) antioxidant pathway.
aimTo investigate the renoprotective effects of AC against DN and elucidate the role of the NRF2/HO-1 pathway.
methodsThe effects of AC on high glucose (HG)-induced proliferation, inflammation, oxidative stress, and fibrosis were evaluated in rat glomerular mesangial cells (HBZY-1)
resultsAC inhibited HG-induced HBZY-1 cell proliferation and significantly improved various indicators of DN in rats, including reduced body weight, and elevated blood glucose, serum creatinine, blood urea nitrogen, and 24-h urine protein. Both
conclusionAC improves DN by reducing inflammation, oxidative stress, and fibrosis through the activation of the NRF2/HO-1 signaling pathway. These findings not only highlight AC as a promising therapeutic candidate for DN but also underscore the potential of targeting the NRF2/HO-1 pathway in developing novel treatments for other chronic kidney diseases characterized by oxidative stress and inflammation.
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