Aim: To evaluate the effect of ginkgolide B treatment on vascular endothelial function in diabetic rats.
Methods: The study included four groups with 15 male Sprague-Dawley rats: control group; control group treated with ginkgolide B; diabetic group; and diabetic treated with ginkgolide B. The activity of superoxide dismutase (SOD), malondialdehyde content, and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunits, and glutathione peroxidase 1 (GPX1) protein expression were determined in aortic tissues. Vasoconstriction to phenylephrine (PHE) and vasorelaxation to acetylcholine (Ach) and sodium nitroprusside (SNP) were assessed in aortic rings. Nitric oxide (NO) and hydrogen sulfide (H2S) were measured, as well as cystathionine γ lyase (CSE) and cystathionine β synthetase (CBS) protein expression, and endothelial nitric oxide synthase (eNOS) activity.
Results: Diabetes significantly impaired PHE-induced vasoconstriction and Ach-induced vasorelaxation (P<0.001), reduced NO bioavailability and H2S production (P<0.001), SOD activity, and GPX1 protein expression (P<0.001), and increased malondialdehyde content and NADPH oxidase subunits, and CSE and CBS protein expression (P<0.001). Ginkgolide B treatment improved PHE vasoconstriction and Ach vasorelaxation (P<0.001), restored SOD (P=0.005) and eNOS (P<0.001) activities, H2S production (P=0.044) and decreased malondialdehyde content (P=0.014). Vasorelaxation to SNP was not significantly different in control and diabetic rats with or without ginkgolide B treatment. Besides, ginkgolide B increased GPX1 protein expression and reduced NADPH oxidase subunits, CBS and CSE protein expression.
Conclusion: Ginkgolide B alleviates endothelial dysfunction by reducing oxidative stress and elevating NO bioavailability and H2S production in diabetic rats.