ArticleFrontiers in pharmacology2024
Astragaloside IV attenuates renal tubule injury in DKD rats via suppression of CD36-mediated NLRP3 inflammasome activation.
Article in Frontiers in pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 14 citations in OpenAlex.
- Mitochondrial Regulation of the NLRP3 Inflammasome in Diabetic Kidney Disease: From Mechanisms to Therapeutic Strategies.International journal of molecular sciences · 2026Review
- [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Wenyang Huazhuo formula extract ameliorates diabetic kidney disease in db/db mice and is associated with modulation of MHC class II molecules and gut microbiota.Frontiers in pharmacology · 2026Article
- Molecular Mechanisms Underlying the Anti-Diabetic Effects of Astragaloside IV: A Focus on Signaling Pathways.Drug design, development and therapy · 2026Review
- Mechanisms of NLRP3 inflammasome in chronic kidney disease and the effects of traditional Chinese medicines.Renal failure · 2025Review
- From Traditional Efficacy to Drug Design: A Review of Astragali Radix.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Transcriptome and single-cell profiling of the mechanism of diabetic kidney disease.World journal of diabetes · 2025Article
- Unveiling macrophage dynamics and efferocytosis-related targets in diabetic kidney disease: insights from single-cell and bulk RNA-sequencing.Frontiers in immunology · 2025Article
- Astragaloside IV Improves Cognitive Impairment by Reducing β-Amyloid and Tau Protein Deposition in Hippocampal Tissue of db/db Mice: A PET/CT Imaging-Based Study.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- Astragaloside IV Improves Diabetic Kidney Disease by Regulating NLRP3 Inflammasome.Journal of diabetes research · 2025Review
- Shenyuan granules improve cellular senescence through Klotho-mediated p16/p21 signaling pathway in diabetic kidney disease.Frontiers in medicine · 2025Article
- Targeting lipid metabolic reprogramming to alleviate diabetic kidney disease: molecular insights and therapeutic strategies.Frontiers in immunology · 2025Review
- The potential biomarker value of soluble CD36 in the treatment of diabetic kidney disease: evidence from GLP-1 and insulin interventions.Frontiers in endocrinology · 2025Observational
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12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: In recent years, diabetic kidney disease (DKD) has emerged as a prominent factor contributing to end-stage renal disease. Tubulointerstitial inflammation and lipid accumulation have been identified as key factors in the development of DKD. Earlier research indicated that Astragaloside IV (AS-IV) reduces inflammation and oxidative stress, controls lipid accumulation, and provides protection to the kidneys. Nevertheless, the mechanisms responsible for its protective effects against DKD have not yet been completely elucidated. Purpose: The primary objective of this research was to examine the protective properties of AS-IV against DKD and investigate the underlying mechanism, which involves CD36, reactive oxygen species (ROS), NLR family pyrin domain containing 3 (NLRP3), and interleukin-1β (IL-1β). Methods: The DKD rat model was created by administering streptozotocin along with a high-fat diet. Subsequently, the DKD rats and palmitic acid (PA)-induced HK-2 cells were treated with AS-IV. Atorvastatin was used as the positive control. To assess the therapeutic effects of AS-IV on DKD, various tests including blood sugar levels, the lipid profile, renal function, and histopathological examinations were conducted. The levels of CD36, ROS, NLRP3, Caspase-1, and IL-1β were detected using western blot analysis, PCR, and flow cytometry. Furthermore, adenovirus-mediated CD36 overexpression was applied to explore the underlying mechanisms through Results: Conclusion: AS-IV alleviated renal tubule interstitial inflammation and tubule epithelial cell apoptosis in DKD rats by inhibiting CD36-mediated lipid accumulation and NLRP3 inflammasome activation.
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