ArticleAntioxidants (Basel, Switzerland)2023
Biochanin A Ameliorates Nephropathy in High-Fat Diet/Streptozotocin-Induced Diabetic Rats: Effects on NF-kB/NLRP3 Axis, Pyroptosis, and Fibrosis.
Article in Antioxidants (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 38 citations in OpenAlex.
- Advances in understanding the NLRP3 inflammasome‑mediated mechanisms and therapeutic targets in diabetic nephropathy (Review).International journal of molecular medicine · 2026Review
- Hsa-miR-5585-3p regulates the NLRP3 activation and the expression of cytokines through CHUK in a cellular model of diabetic kidney disease.BMC endocrine disorders · 2026Article
- Targeting pyroptosis in renal fibrosis: From molecular mechanisms to therapeutic horizons (Review).International journal of molecular medicine · 2026Review
- Post‑translational modifications in diabetic kidney disease (Review).International journal of molecular medicine · 2026Review
- Gut microbiota implication in diabetic kidney disease: mechanisms and novel therapeutic strategies.Renal failure · 2025Review
- Research Progress on Signalling Pathways Related to Sepsis-Associated Acute Kidney Injury in Children.Current issues in molecular biology · 2025Review
- Puerarin raises exosomal miR- 342 - 3p by inhibiting lncRNA NEAT1 in umbilical cord mesenchymal stem cells to alleviate renal tubular epithelial cell pyroptosis in chronic renal failure.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Natural compounds attenuate combined chromium and arsenic-induced oxidative stress and nephritic apoptosis by activating the Nrf2/Keap1 signaling and associated xenobiotic metabolizing enzymes.Scientific reports · 2025Article
- Targeting NF-κB in diabetic nephropathy: exploring the therapeutic potential of phytoconstituents.Archives of pharmacal research · 2025Review
- Programmed Cell Death in Diabetic Kidney Disease: Mechanisms and Therapeutic Targeting.Journal of inflammation research · 2025Review
- Yiqi Huoxue recipe ameliorates diabetic nephropathy by mediating VAPB-PTPIP51 complex to activate autophagy and regulate MAM contact.Frontiers in nutrition · 2025Article
- NLRP3 Inflammasome-Mediated Pyroptosis in Diabetic Nephropathy: Pathogenic Mechanisms and Therapeutic Targets.Journal of inflammation research · 2025Review
- Pyroptosis: An Accomplice in the Induction of Multisystem Complications Triggered by Obstructive Sleep Apnea.Biomolecules · 2024Review
- Research Progress of Pyroptosis in Diabetic Kidney Disease.International journal of molecular sciences · 2024Review
- Harnessing the Power of Polyphenols: A New Frontier in Disease Prevention and Therapy.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Article
- A Novel Bioswitchable miRNA Mimic Delivery System: Therapeutic Strategies Upgraded from Tetrahedral Framework Nucleic Acid System for Fibrotic Disease Treatment and Pyroptosis Pathway Inhibition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Potential Benefits of Antioxidant Phytochemicals in Type 2 Diabetes.Molecules (Basel, Switzerland) · 2023Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Nephropathy is the most prevalent microvascular disorder in diabetes mellitus. Oxidative stress and inflammatory cascade provoked by the persistent hyperglycemic milieu play integral roles in the aggravation of renal injury and fibrosis. We explored the impact of biochanin A (BCA), an isoflavonoid, on the inflammatory response, nod-like receptor protein 3 (NLRP3) inflammasome activation, oxidative stress, and fibrosis in diabetic kidneys. A high-fat-diet/streptozotocin (HFD/STZ)-induced experimental model of diabetic nephropathy (DN) was established in Sprague Dawley rats, and in vitro studies were performed in high-glucose-induced renal tubular epithelial (NRK-52E) cells. Persistent hyperglycemia in diabetic rats was manifested by perturbation of renal function, marked histological alterations, and oxidative and inflammatory renal damage. Therapeutic intervention of BCA mitigated histological changes, improved renal function and antioxidant capacity, and suppressed phosphorylation of nuclear factor-kappa B (NF-κB) and nuclear factor-kappa B inhibitor alpha (IκBα) proteins. Our in vitro data reveal excessive superoxide generation, apoptosis, and altered mitochondrial membrane potential in NRK-52E cells that were cultured in a high-glucose (HG) environment were subsided by BCA intervention. Meanwhile, the upregulated expressions of NLRP3 and its associated proteins, the pyroptosis-indicative protein gasdermin-D (GSDMD) in the kidneys, and HG-stimulated NRK-52E cells were significantly ameliorated by BCA treatment. Additionally, BCA blunted transforming growth factor (TGF)-β/Smad signaling and production of collagen I, collagen III, fibronectin, and alfa-smooth muscle actin (α-SMA) in diabetic kidneys. Our results indicate the plausible role of BCA in attenuating DN, presumably through modulation of the apoptotic cascade in renal tubular epithelial cells and the NF-κB/NLRP3 axis.
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Registered trials
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