Bacopa monniera prevents from aluminium neurotoxicity in the cerebral cortex of rat brain.
Bacopa monniera is a perennial herb, and is used as a nerve tonic in äyurveda, a traditional medicinal system in India. Aluminium-induced neurotoxicity is well known and different salts of aluminium have been reported to accelerate oxidative damage to biomolecules like lipids, proteins and nucleic acids. The objective of the present study was to investigate whether Bacopa monniera could potentially inhibit aluminium toxicity in the cerebral cortex. Male Wister rats (8 months old) were administered with AlCl(3) orally at a dose of 50mg/kg/day in drinking water for 1 month. Experimental rats were given AlCl(3) along with Bacopa monniera extract at a dose of 40 mg/kg/day. One group of rats was treated with l-deprenyl at a dose of 1mg/kg/day along with AlCl(3) treatment. We have observed that Bacopa monniera prevented accumulation of lipid and protein damage significantly, which resulted from aluminium intake. Decline in the activity of endogenous antioxidant enzymes associated with aluminium administration was also inhibited by Bacopa monniera extract. The potential of Bacopa monniera to inhibit Al-induced oxidative stress was observed to be similar to that of l-deprenyl, which was taken as standard. The potential of Bacopa monniera extract to prevent aluminium neurotoxicity was reflected at the microscopic level as well, indicative of its neuroprotective effects. These findings strongly implicate that Bacopa monniera has potential to protect brain from oxidative damage resulting from aluminium toxicity.
Jyoti
Amar
A
Neurobiology Laboratory, School of Life Sciences, Jawaharlal Nehru University, New Delhi, India.
Sethi
Pallavi
P
Sharma
Deepak
D
D000447:Aldehydes / Q000378:metabolism; D000077410:Aluminum Chloride; D017607:Aluminum Compounds; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology* / Q000627:therapeutic use; D034681:Bacopa; D002540:Cerebral Cortex / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D002712:Chlorides; D004195:Disease Models, Animal; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D007194:India; D015227:Lipid Peroxidation / Q000187:drug effects*; D008297:Male; D008515:Medicine, Ayurvedic; D018696:Neuroprotective Agents / Q000494:pharmacology* / Q000627:therapeutic use; D020258:Neurotoxicity Syndromes / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D018384:Oxidative Stress / Q000187:drug effects*; D010936:Plant Extracts / Q000494:pharmacology; D050050:Protein Carbonylation / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D012642:Selegiline / Q000494:pharmacology; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
D000447:Aldehydes; D017607:Aluminum Compounds; D000975:Antioxidants; D002712:Chlorides; D018696:Neuroprotective Agents; D010936:Plant Extracts; D017392:Thiobarbituric Acid Reactive Substances; D012642:Selegiline; D000077410:Aluminum Chloride; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005982:Glutathione Transferase; D005978:Glutathione; C027576:4-hydroxy-2-nonenal