ArticleSichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition2025
Targeted Delivery of Triptolide Alleviates Diabetic Nephropathy via Inactivation of JAK2-STAT1 Signaling.
Article in Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition, 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.
- The expression patterns of Interleukin-26, Interleukin-35, and signal transducer and activator of transcription 1 in Type1 diabetes patients with diabetic nephropathy.Molecular biology reports · 2026Article
- Mechanisms of Macrophage Glycolytic Reprogramming and Interventional Effects of Traditional Chinese Medicine on Renal Fibrosis.International journal of general medicine · 2026Review
- The Mechanism and Application of Traditional Chinese Medicine Nano-Formulations in the Treatment of Renal Fibrosis.International journal of nanomedicine · 2026Review
- Research progress on the regulatory effects and mechanisms of natural active products on intestinal barrier function.Frontiers in pharmacology · 2025Review
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Authors and funding
6 authors.
Funding
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Abstract
Objective: Inflammation and fibrosis are key features of diabetic nephropathy (DN). Triptolide (TP) exhibits anti-inflammatory and anti-fibrotic properties, though its mechanisms of action in DN remain unclear. CREKA (Cys-Arg-Glu-Lys-Ala) is a pentapeptide that specifically binds to fibronectin (FN), and the CREKA-modified liposome (CREKA-Lip) represents a novel FN-targeted drug delivery system. This study aimed to investigate the role of TP in diabetic db/db mice and determine whether encapsulation within CREKA-Lip enhances therapeutic efficacy while reducing the multi-organ toxicity of TP. Methods: Eight-week-old diabetic db/db mice received tail vein injections twice weekly with vehicle, free TP, or CREKA-Lip/TP for 10 weeks. Urine and serum parameters were measured, and kidney, heart, liver, and testis tissues were collected for pathological evaluation. Protein-protein interaction networks were constructed using Cytoscape and its plug-ins to identify core targets and elucidate the therapeutic mechanism of TP against DN. Inflammatory, fibrotic, apoptotic, and lipid metabolism markers were evaluated in the kidneys of diabetic mice with DN and in high glucose-treated mouse mesangial cells and podocytes using qPCR, Western blot, immunohistochemistry, and immunofluorescence assays. Results: TP administration reduced fasting blood glucose levels and glomerular mesangial expansion in diabetic mice. TP significantly suppressed renal inflammation, fibrosis, and apoptosis while enhancing lipid metabolism. Integration of network pharmacology, molecular docking, and transcriptomics revealed that TP ameliorated DN by inhibiting the JAK2-STAT1 signaling pathway. Conclusion: TP improves renal inflammation, fibrosis, apoptosis, and lipid homeostasis, thereby ameliorating DN by inhibiting JAK2-STAT1 activation. Targeted delivery of TP via FN-binding CREKA-Lip enhances therapeutic efficacy while minimizing multi-organ toxicity.
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