Neuroprotective effect of Allium cepa L. in aluminium chloride induced neurotoxicity.
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 (PPARγ 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 PPARγ receptor agonism has also been suggested as a putative neuroprotective mechanism of A. cepa, which needs further studies for confirmation.
Department of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala, 147002 Punjab, India.
Tanveer
T
Singh
Department of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala, 147002 Punjab, India. Electronic address: goelrkpup@gmail.com.
Rajesh Kumar
RK
Goel
D000110:Acetylcholinesterase / Q000378:metabolism; D000077410:Aluminum Chloride; D017607:Aluminum Compounds / Q000633:toxicity*; D000818:Animals; D001362:Avoidance Learning / Q000187:drug effects; D001921:Brain / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D002712:Chlorides / Q000633:toxicity*; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D005978:Glutathione / Q000378:metabolism; D008297:Male; D008568:Memory / Q000187:drug effects; D051379:Mice; D009119:Muscle Contraction / Q000187:drug effects; D018696:Neuroprotective Agents / Q000494:pharmacology / Q000627:therapeutic use*; D020258:Neurotoxicity Syndromes / Q000188:drug therapy* / Q000209:etiology*; D009566:Nitrates / Q000378:metabolism; D019697:Onions / Q000737:chemistry*; D010936:Plant Extracts / Q000494:pharmacology / Q000627:therapeutic use*; D045442:Rotarod Performance Test; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
D017607:Aluminum Compounds; D002712:Chlorides; D018696:Neuroprotective Agents; D009566:Nitrates; D010936:Plant Extracts; D017392:Thiobarbituric Acid Reactive Substances; D000077410:Aluminum Chloride; D002374:Catalase; D000110:Acetylcholinesterase; D005978:Glutathione
Allium cepa; Aluminium; Memory deficit; Neurotoxicity; PPARγ