| Autor: |
Asiwe JN; Department of Physiology, PAMO University of Medical Sciences, Port-Harcourt, Nigeria.; Department of Physiology, University of Ibadan, Ibadan, Nigeria., Yovwin GD; Department of Family Medicine, Delta State University, Abraka, Nigeria., Ekene NE; Department of Pharmacology, Rivers State University, Port-Harcourt, Nigeria., Ovuakporaye SI; Department of Physiology, Delta State University, Abraka, Nigeria., Nnamudi AC; Department of Biochemistry, PAMO University of Medical Sciences, Port-Harcourt, Nigeria., Nwangwa EK; Department of Physiology, Delta State University, Abraka, Nigeria. |
| Abstrakt: |
This study investigated the modulatory effect of Ginkgo biloba extract on lead acetate-induced endothelial dysfunction. Animals were administered GBE (50 mg/kg and 100 mg/kg orally) after exposures to lead acetate (25 mg/kg orally) for 14 days. Aorta was harvested after euthanasia, the tissue was homogenised, and supernatants were decanted after centrifuging. Oxidative, nitrergic, inflammatory, and anti-apoptotic markers were assayed using standard biochemical procedure, ELISA, and immunohistochemistry, respectively. GBE reduced lead-induced oxidative stress by increasing SOD, GSH, and CAT as well as reducing MDA levels in endothelium. Pro-inflammatory cytokines (TNF-α and IL-6) were reduced while increasing Bcl-2 protein expression. GBE lowered endothelin-I and raised nitrite levels. Histological changes caused by lead acetate were normalised by GBE. Our findings suggest that Ginkgo biloba extract restored endothelin-I and nitric oxide functions by increasing Bcl-2 protein expression and reducing oxido-inflammatory stress in endothelium. |
