title: Beneficial anti-Parkinson effects of camel milk in Chlorpromazineinduced animal model: Behavioural and histopathological study.
abstract: Potential roles of natural products have been identified for preventing or treating various diseases. Our aim was to investigate the effectiveness of camel milk in an animal model of Parkinson's disease and compare it with standard treatment (levodopa + carbidopa combination). 40 Wistar albino rats weighing 200-250 gram were divided into four groups of 10 animals each. Group I was kept on water and served as normal control, group II served as negative control, treated with chlorpromazine (5mg/kg i.p.), group III was given camel milk (33ml/kg p.o) and group IV the standard combination of levodopa + carbidopa (100+10mg/kg) respectively, 30 minutes after chlorpromazine treatment. All animals were subjected to the drugs treatment for 30 days. Catalepsy was assessed by Bar test on day 21 and day 30 at 30, 60, 90 and 120 minutes interval. On 30th day animals were sacrificed and whole brains were examined for histopathological changes. The results revealed highly significant (p<0.001) anti-cataleptic effect of camel milk on day 21 and 30 in comparison to chlorpromazine. When compared with standard therapy, the results showed that anti-Parkinson's activity of camel milk was significant (p<0.01) on day 21. However, the difference in activity was non-significant on day 30. Histopathology of the brain showed that administration of camel milk reveals intact architecture with mild degenerative changes than chlorpromazine and levodopa + carbidopa treated animals. In conclusion, camel milk possesses anti-Parkinson's activity. However, its long term efficacy and safety needs to be evaluated clinically.
authors.affiliation: Faculty of Pharmacy, Jinnah University for Women, Karachi, Pakistan.
authors.forename: Humera
authors.initials: H
authors.lastname: Khatoon
authors.affiliation: Department of Pharmacology, Faculty of Pharmacy, University of Karachi, Pakistan.
authors.forename: Rahela
authors.initials: R
authors.lastname: Najam
authors.affiliation: Department of Pathology, DOW University of Health Sciences, Karachi, Pakistan / DOW Research Institute of Biotechnology and Biomedical Sciences, DOW University of Health Sciences, Karachi, Pakistan.
authors.forename: Talat
authors.initials: T
authors.lastname: Mirza
authors.affiliation: Department of Pathology, DOW University of Health Sciences, Karachi, Pakistan.
authors.forename: Bushra
authors.initials: B
authors.lastname: Sikandar
mesh_terms: D000818:Animals; D000978:Antiparkinson Agents / Q000494:pharmacology; D001522:Behavior, Animal / Q000187:drug effects*; D001921:Brain / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology; D002162:Camelus; D002230:Carbidopa / Q000494:pharmacology; D002375:Catalepsy / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control; D002746:Chlorpromazine; D004338:Drug Combinations; D005260:Female; D007980:Levodopa / Q000494:pharmacology; D008297:Male; D008892:Milk; D020734:Parkinsonian Disorders / Q000139:chemically induced / Q000473:pathology / Q000517:prevention & control* / Q000523:psychology; D017208:Rats, Wistar; D013997:Time Factors
chemical_list: D000978:Antiparkinson Agents; D004338:Drug Combinations; C009265:carbidopa, levodopa drug combination; D007980:Levodopa; D002230:Carbidopa; D002746:Chlorpromazine