ArticlePflugers Archiv : European journal of physiology2023
Ginkgolide B caused the activation of the Akt/eNOS pathway through the antioxidant effect of SOD1 in the diabetic aorta.
Article in Pflugers Archiv : European journal of physiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Dietary Supplementation with GBE and TP Alleviates Heat Stress-Induced Lung Oxidative Damage in Broilers.Animals : an open access journal from MDPI · 2026Article
- The Effects of a Novel Nutraceutical Composition Containing Coenzyme QFood science & nutrition · 2025Article
- Inhibition of microRNA-139-5p by glucagon-like peptide-1 ameliorates oxidative stress-induced vascular endothelial cell damage via targeting SOD1/GCLc.Endocrine connections · 2025Article
- Exploring the multifaceted role of ginkgolides and bilobalide fromFood science and biotechnology · 2024Review
- Mechanisms of Flavonoids and Their Derivatives in Endothelial Dysfunction Induced by Oxidative Stress in Diabetes.Molecules (Basel, Switzerland) · 2024Review
- Macrophage immunometabolism in diabetes-associated atherosclerosis.Immunometabolism (Cobham, Surrey) · 2023Review
- Research Progress of Flavonoids Regulating Endothelial Function.Pharmaceuticals (Basel, Switzerland) · 2023Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ginkgo biloba extract (GBE) helps lower cardiovascular disease risk. Diabetes mellitus (DM)-induced endothelial dysfunction is a critical and initiating factor in the beginning of diabetic vascular complications. It was reported that GBE causes an endothelial-dependent relaxation. This study was designed to figure out the molecular basis on which GBE protects from endothelial dysfunction in diabetes because the underlying mechanisms are unclear. Studies were performed in a normal control group and streptozotocin/nicotinamide-induced DM group. In aortas, notably diabetic aortas, GBE, and ginkgolide B (GB), a constituent of GBE, produced a dose-dependent relaxation. The relaxation by GB was abolished by prior incubation with L-NNA (an endothelial nitric oxide synthase (NOS) inhibitor), LY294002 (a phosphoinositide 3-kinase (PI3K) inhibitor), and Akt inhibitor, confirming the essential role of PI3K/Akt/eNOS signaling pathway. We also demonstrated that GB induced the phosphorylation of Akt and eNOS in aortas. The superoxide dismutase1 (SOD1) expression level decreased in DM aortas, but GB stimulation increased SOD activity and SOD1 expression in DM aortas. Our novel findings suggest that in DM aortas, endothelial-dependent relaxation induced by GB was mediated by activation of SOD1, resulting in activation of the Akt/eNOS signaling pathway.
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