ArticleScientific reports2025
Mechanism of dracorhodin in accelerating diabetic foot ulcer healing via the Nrf2 pathway, a network pharmacology, molecular docking and experimental validation.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- 4-Methylumbelliferone for type 1 diabetes therapy: evidence for β-cell protection via EGFR/PI3K/Akt signaling.Journal of endocrinological investigation · 2026Article
- Curcumin-Dragon's blood-chitosan nanosuspension for dual forensic detection.Scientific reports · 2026Article
- The Role of Ferroptosis in Diabetes Pathogenesis: Therapeutic Implications of Hydrogen Sulfide and Its Reactive Metabolites.Antioxidants (Basel, Switzerland) · 2026Review
- Crosstalk between oxidative stress and inflammatory pathways: Natural therapeutic approaches for diabetic wound healing.World journal of diabetes · 2025Review
- Ferroptosis in diabetes mellitus and its complications: overview of clinical and preclinical research.Cell death discovery · 2025Review
- Targeting diabetic foot ulcer pathophysiology: altered signaling pathways and 3D scaffold as an emerging treatment strategy.3 Biotech · 2025Review
- Revealing the Multi-Target Mechanisms of Fespixon Cream in Diabetic Foot Ulcer Healing: Integrated Network Pharmacology, Molecular Docking, and Clinical RT-qPCR Validation.Current issues in molecular biology · 2025Article
- Advanced Natural Therapeutics and Delivery Strategies for Diabetic Foot Ulcers: A Mini Review.Drug design, development and therapy · 2025Review
- Management of diabetic foot ulcers: polyherbal formulations and novel delivery systems for herbal active components.Frontiers in pharmacology · 2025Review
- Understanding risk factors and prognosis in diabetic foot ulcers.Open life sciences · 2025Review
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10 authors.
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Abstract
Delayed wound healing in diabetic foot ulcer (DFU) is a major cause of amputations, with ferroptosis impeding recovery. Dracorhodin (DP), a flavonoid from Dragon's Blood, has shown anti-inflammatory and wound-healing properties, though its molecular mechanisms is unclear. This study investigates DP's role in DFU treatment through bioinformatics and experimental approaches. A rat model of DFU was created with a high-fat/high-glucose diet and streptozotocin (STZ) induction, and wound healing was monitored after applying varying DP doses. Histopathological analysis and ELISA assessed tissue changes, inflammatory markers, and growth factors. Network pharmacology and molecular docking were used to identify core targets and pathways, while human umbilical vein endothelial cells (HUVECs) were used for in vitro testing. The results demonstrated that DP accelerated wound healing in DFU rats in a dose-dependent manner by enhancing collagen synthesis, angiogenesis, and growth factor levels, while simultaneously reducing inflammation and ROS levels. Network pharmacology and molecular docking analyses identified the Nrf2-mediated ferroptosis pathway as a potential key mechanism underlying DP's therapeutic effects in DFU. In vitro experiments further revealed that DP improved cell viability and migration, while decreasing ROS and lipid peroxidation levels, effects attributed to Nrf2 pathway activation. These outcomes were significantly attenuated by the Nrf2 inhibitor ML385. In conclusion, DP promotes DFU healing via activation of the Nrf2 pathway and inhibition of ferroptosis.
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