POSSIBLE NEUROPROTECTIVE EFFECTS OF CROCIN AGAINST MOTOR AND NEUROCHEMICAL CHANGES IN ROTENONE INDUCED ANIMAL MODEL OF PARKINSON'S DISEASE

Abstract

Parkinson’s disease (PD) is considered the second most common neurodegenerative disease with subsequent motor and behavioral deficits. Oxidative stress plays a key role in the pathogenesis of PD. AIM: The aim of this study was to investigate the possible neuroprotective effects of crocin on rotenone-induced Parkinson- like behaviors. MATERIALS M (2) Crocin 40 (10 rats); (3) Polyethylene glycol (PEG) (10 rats) ; (4) Rotenone (40 rats) injected I.P. of 1.5 mg/kg/48 hrs. for 2 weeks [11]; Preliminary behavioral tests and the rats that showed PD features were randomly subdivided into 4 equal groups of 10 rats per each. (4A) Rotenone-treated: (4B): Crocin 20 treated. (4C): Crocin 40 treated. (4D) L-DOPA treated- group. The neurobehavioral were done. In serum, the level of 8-hydroxydeoxyguanosine 8-OHdG was estimated. The level of malondialdehyde (MDA), reduced glutathione (GSH), tumor necrosis factor alpha TNF-α, dopamine, and nitrite/ nitrate levels were measured in the brain tissue. RESULTS: Rotenone induced neurobehavioral deficits with elevation of brain MDA, brain TNF- α, Nitrite/nitrate level and serum 8-OHdG and reduction of GSH, brain tissue dopamine. Crocin (20 or 40) improved these neurobehavioral deficits. Crocin (20 or 40) and L-DOPA decreased MDA, serum 8-OHdG, TNF- α and Nitrite/nitrate level and increased GSH and dopamine level. Crocin 40 had achieved potent effect compared with crocin 20. In summary, rotenone-induced Parkinson- like behavior in rats. Crocin achieved a protective effect