ArticleApplied biochemistry and biotechnology2025
Astragaloside IV Relieves Mitochondrial Oxidative Stress Damage and Dysfunction in Diabetic Mice Endothelial Progenitor Cells by Regulating the GSK-3β/Nrf2 Axis.
Article in Applied biochemistry and biotechnology, 2025. 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.
- Natural Small Molecules Targeting Mitochondrial Quality Control for the Treatment of Metabolic Diseases: Mechanisms, Novel Formulations, and Translational Perspectives.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Molecular Mechanisms Underlying the Anti-Diabetic Effects of Astragaloside IV: A Focus on Signaling Pathways.Drug design, development and therapy · 2026Review
- Astragaloside IV in type 2 diabetic vascular complications: from traditional mechanisms to an emerging epitranscriptomic (m6A) perspective.American journal of translational research · 2026Review
- The HO-1/bilirubin axis in cardiovascular protection: critical evidence for modulation by plant metabolites and traditional multi-component formulations used in Chinese medicine.Frontiers in pharmacology · 2026Review
- When Mitochondria Falter, the Barrier Fails: Mechanisms of Inner Blood-Retinal Barrier (iBRB) Injury and Opportunities for Mitochondria-Targeted Repair.International journal of molecular sciences · 2025Review
- Research Progress on Chemical Components ofMolecules (Basel, Switzerland) · 2025Review
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Authors and funding
12 authors.
Funding
Abstract
Dysregulation of mitochondrial activity is a major cause of diabetes mellitus (DM) and its complications. Astragaloside IV, a natural herbal product, possesses protective properties against DM. This study aimed to evaluate how astragaloside IV affects oxidative stress and mitochondrial function in endothelial progenitor cells (EPCs) and elucidate the underlying mechanisms. A high glucose (HG)-induced human EPC (hEPC) model and a streptozotocin (STZ)-induced DM mouse model were established to investigate the effects of astragaloside IV on EPC function and wound healing in the context of DM. In HG-exposed hEPCs, astragaloside IV reduced apoptosis and increased cell viability and tube formation (P < 0.05). In STZ-induced DM mice, astragaloside IV promoted wound healing and increased the expression of the endothelial marker CD31 (P < 0.05) in wound tissues. In addition, the regulation of oxidative damage and mitochondrial dysfunction by astragaloside IV was investigated. We found that astragaloside IV attenuated mitochondrial damage, decreased ROS and mtROS levels (P < 0.05), decreased MDA activity and enhanced SOD activity (P < 0.05), and downregulated DPR1 levels and upregulated MFN1, MFN2, and OPA1 levels (P < 0.05). Mechanistically, the potential involvement of GSK-3β/Nrf2 was investigated by molecular docking and intervention with the GSK-3β activator sodium nitroprusside (SNP). Astragaloside IV was confirmed to dock with GSK-3β, and it increased the phosphorylation of GSK-3β (P < 0.05) and the expression of Nrf2 as well as its downstream factors HO-1 and NQO1 (P < 0.05). SNP reversed the protective effects of astragaloside IV. These results indicated that astragaloside IV attenuated HG- and STZ-induced injury through the GSK-3β/Nrf2 pathway. These results revealed that astragaloside IV may have the potential to be an active component for protection against DM and its complications.
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