Neuroprotective role of 6-Gingerol-rich fraction of Zingiber officinale (Ginger) against acrylonitrile-induced neurotoxicity in male Wistar rats

Author:

Farombi Ebenezer Olatunde1,Abolaji Amos Olalekan2,Adetuyi Babatunde Oluwafemi2,Awosanya Olaide2,Fabusoro Mobolaji2

Affiliation:

1. Molecular Drug Metabolism and Toxicology Research Laboratories , Department of Biochemistry, Faculty of Basic Medical Sciences , College of Medicine, University of Ibadan , Ibadan , Nigeria , Phone: +2348023470333, Fax: 234-2-8103043

2. Molecular Drug Metabolism and Toxicology Research Laboratories , Department of Biochemistry, Faculty of Basic Medical Sciences , College of Medicine, University of Ibadan , Ibadan , Nigeria

Abstract

Abstract Background Acrylonitrile (AN) is a neurotoxin that is widely used to manufacture synthetic fibres, plastics and beverage containers. Recently, we reported the ameliorative role of 6-gingerol-rich fraction from Zingiber officinale (Ginger, GRF) on the chlorpyrifos-induced toxicity in rats. Here, we investigated the protective role of GRF on AN-induced brain damage in male rats. Methods Male rats were orally treated with corn oil (2 mL/kg, control), AN (50 mg/kg, Group B), GRF (200 mg/kg, Group C), AN [50 mg/kg+GRF (100 mg/kg) Group D], AN [(50 mg/kg)+GRF (200 mg/kg) Group E] and AN [(50 mg/kg)+N-acetylcysteine (AC, 50 mg/kg) Group F] for 14 days. Then, we assessed the selected markers of oxidative damage, antioxidant status and inflammation in the brain of rats. Results The results indicated that GRF restored the AN-induced elevations of brain malondialdehyde (MDA), interleukin-6 (IL-6), tumour necrosis factor-α (TNF-α) and Nitric Oxide (NO) levels. GRF also prevented the AN-induced depletion of brain glutathione (GSH) level and the activities of Glutathione S-transferase (GST), glutathione peroxidase (GPx) and superoxide dismutase (SOD) in rats (p<0.05). Furthermore, GRF prevented the AN-induced cerebral cortex lesion and increased brain immunohistochemical expressions of Caspases-9 and -3. Conclusions Our data suggest that GRF may be a potential therapeutic agent in the treatment of AN-induced model of brain damage.

Publisher

Walter de Gruyter GmbH

Subject

Drug Discovery,Pharmacology,General Medicine,Physiology

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