期刊
NEUROTOXICOLOGY
卷 49, 期 -, 页码 1-7出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.neuro.2015.04.007
关键词
Aluminium; Neurotoxicity; Allium cepa; Memory deficit; PPAR gamma
资金
- Department of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala
- Department of Biotechnology, New Delhi, India [BT/PR4548/INF/22/146/2012]
The present study was envisaged to investigate the neuroprotective potential of Allium cepa (A. cepa) in aluminium chloride induced neurotoxicity. Aluminium chloride (50 mg/kg/day) was administered orally in mice supplemented with different doses of A. cepa hydroethanolic extract for a period of 60 days. Various behavioural, biochemical and histopathological parameters were estimated in aluminium exposed animals. Chronic aluminium administration resulted in significant motor incoordination and memory deficits, which were also endorsed biochemically as there was increased oxidative stress as well as elevated acetylcholinesterase (AChE) and aluminium levels in the brain. Supplementation with A. cepa in aluminium exposed animals significantly improved muscle coordination and memory deficits as well as reduced oxidative stress, AChE and decreased abnormal aluminium deposition in the brain. Histopathologically, there was marked deterioration visualized as decreased vacuolated cytoplasm as well as decreased pyramidal cells in the hippocampal area of mice brain which were found to be reversed with A. cepa supplementation. Administration of BADGE (PPAR gamma antagonist) in aluminium exposed animals reversed the neuroprotective potential of A. cepa as assessed with various behavioural, biochemical, neurochemical and histopathological estimations. In conclusion, finding of this study suggested significant neuroprotective potential of A. cepa in aluminium induced neurotoxicity. Further, the role of PPAR gamma receptor agonism has also been suggested as a putative neuroprotective mechanism of A. cepa, which needs further studies for confirmation. (C) 2015 Elsevier Inc. All rights reserved.
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