Neuroprotective role of Ginkgo biloba against cognitive deficits associated with Bisphenol A exposure: An animal model study.

Autor: El Tabaa MM; Environmental Studies & Research Institute (ESRI), University of Sadat City, Egypt. Electronic address: manar.eltabaa@esri.usc.edu.eg., Sokkar SS; Pharmacology and Toxicology Department, Faculty of Pharmacy, Tanta University, Egypt. Electronic address: samya.sokar@pharm.tanta.edu.eg., Ramadan ES; Psychiatry Department, Faculty of Medicine, Tanta University, Egypt. Electronic address: ehab_ramadan@yahoo.com., Abd El Salam IZ; Environmental Studies & Research Institute (ESRI), University of Sadat City, Egypt. Electronic address: inas.abdelsalam@esri.usc.edu.eg., Zaid A; Pathology Department, Faculty of Veterinary Medicine, University of Sadat City, Egypt. Electronic address: aniszaid@vet.usc.edu.eg.
Jazyk: angličtina
Zdroj: Neurochemistry international [Neurochem Int] 2017 Sep; Vol. 108, pp. 199-212. Date of Electronic Publication: 2017 Mar 31.
DOI: 10.1016/j.neuint.2017.03.019
Abstrakt: Our study aimed to elucidate to what extent Ginkgo biloba (Gb) can protect rats from cognitive deficits induced by exposure to Bisphenol A (BPA) at high dose. Therefore, sixty male Wistar rats were randomly divided into four groups of 15 animals in each group: Vehicle group, Gb-control group, BPA-exposed group and Gb pre-treated group. All administrations were given daily by an oral gavage once a day for eight weeks. Cognitive function was assessed using Morris water maze; Y-maze and Novel object recognition tasks. Additionally, hippocampal levels of DA, NE and 5-HT were measured. BPA-induced oxidative stress was evaluated by determining SOD activity, NO and MDA levels in rat hippocampus as well as level of circulating adiponectin. Moreover, histopathological changes in CA3 region of rat hippocampus and immunohistochemical expression of NF-κB and Caspase-3 were investigated. We found that Gb pretreatment significantly improved cognitive performance; may be via increasing hippocampal levels of estrogen-dependent biogenic amines. At the same time, Gb could strictly control BPA-induced oxidative stress by improving SOD activity and adiponectin level with decrease in NO and MDA levels. Lastly, Gb alleviated the histopathological injuries induced by BPA and inhibited NF-κB and caspase-3 activation. In conclusion, our results suggested that Gb has potential to ameliorate BPA-induced hippocampal neuronal damage and subsequent cognitive deficits through mechanisms involving its ability to enhance the release of biogenic amines as well as its antioxidant and adiponectin pro-secretory effects.
(Copyright © 2017 Elsevier Ltd. All rights reserved.)
Databáze: MEDLINE
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