Ginkgo biloba modulates ET-I/NO signalling in Lead Acetate induced rat model of endothelial dysfunction: Involvement of oxido-inflammatory mediators

• Published in: International journal of environmental health research Vol. 34; no. 2; pp. 979 - 990
• Main Authors: Asiwe, Jerome Ndudi, Yovwin, Godwin D., Ekene, Nwoke Enekabokom, Ovuakporaye, Simon Irikefe, Nnamudi, Anthony Chibuzor, Nwangwa, Eze Kingsley
• Format: Journal Article
• Language: English
• Published: England Taylor & Francis 01.02.2024; Taylor & Francis LLC
• Subjects: Acetates; Animals; Aorta; Apoptosis; Bcl-2 protein; Decantation; endothelial dysfunction; Endothelins; Endothelium; Enzyme-linked immunosorbent assay; Ginkgo biloba; Ginkgo Extract; Immunohistochemistry; Inflammation; Lead; lead acetate; Lead acetates; Nitric oxide; Oxidative stress; oxido-inflammatory stress; Plant Extracts - pharmacology; Proteins; Proto-Oncogene Proteins c-bcl-2; Rats; Tumor necrosis factor-α; Ginkgo biloba; apoptosis; endothelial dysfunction; oxido-inflammatory stress; lead acetate
• ISSN: 0960-3123; 1369-1619
• DOI: 10.1080/09603123.2023.2194612

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.