Neuroprotection by crocetin in a hemi-parkinsonian rat model.
Reactive oxygen species (ROS) are implicated as the leading biochemical cause of neuronal death in various neurologic disorders, including Parkinson's disease. In the present study, neuromodulatory effects of crocetin (active constituent of Crocus sativus) in a 6-hydroxydopamine (6-OHDA) model of rat Parkinsonism were investigated. Male Wistar rats were pre-treated with crocetin (25, 50 and 75 microg/kg body weight) for 7 days and subjected to unilateral intrastriatal injection of 10 microg 6-OHDA on day 8. Locomotion and rotation were observed on day 23 post-injection, and after 4 weeks, striatum and substantia nigra were dissected out by decapitation. Activity of antioxidant enzymes and content of dopamine (DA) and its metabolites were estimated in striatum, whereas glutathione (GSH) content and thiobarbituric acid reactive substance (TBARS) were evaluated in substantia nigra. Levels of GSH and dopamine were protected, while TBARS content was attenuated in crocetin-treated groups. The activity of antioxidant enzymes was decreased in the lesion group, but protected in the crocetin-treated groups. These findings were supported by the histopathologic findings in the substantia nigra that showed that crocetin protects neurons from deleterious effects of 6-OHDA. This study revealed that crocetin, which is an important ingredient of diet in India and also used in various systems of indigenous medicine, is helpful in preventing Parkinsonism and has therapeutic potential in combating this devastating neurologic disorder.
Ahmad
Abdullah Shafique
AS
Neurotoxicology Laboratory, Department of Medical Elementology and Toxicology, Jamia Hamdard (Hamdard University), Hamdard Nagar, New Delhi-110062, India.
Ansari
Mubeen Ahmad
MA
Ahmad
Muzamil
M
Saleem
Sofiyan
S
Yousuf
Seema
S
Hoda
Md Nasrul
MN
Islam
Fakhrul
F
D015102:3,4-Dihydroxyphenylacetic Acid / Q000378:metabolism; D000704:Analysis of Variance; D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects; D002338:Carotenoids / Q000494:pharmacology*; D002374:Catalase / Q000378:metabolism; D003342:Corpus Striatum / Q000187:drug effects / Q000378:metabolism; D004195:Disease Models, Animal; D004298:Dopamine / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D006719:Homovanillic Acid / Q000378:metabolism; D008297:Male; D009043:Motor Activity / Q000187:drug effects; D018696:Neuroprotective Agents / Q000494:pharmacology*; D016627:Oxidopamine / Q000633:toxicity; D010302:Parkinson Disease, Secondary / Q000139:chemically induced / Q000503:physiopathology / Q000517:prevention & control*; D051381:Rats; D017208:Rats, Wistar; D013378:Substantia Nigra / Q000187:drug effects / Q000473:pathology; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014801:Vitamin A / Q000031:analogs & derivatives
D018696:Neuroprotective Agents; D017392:Thiobarbituric Acid Reactive Substances; C487773:trans-sodium crocetinate; D015102:3,4-Dihydroxyphenylacetic Acid; D014801:Vitamin A; D002338:Carotenoids; D016627:Oxidopamine; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D005978:Glutathione; D004298:Dopamine; D006719:Homovanillic Acid