Neuroprotective effect of curcumin-I in copper-induced dopaminergic neurotoxicity in rats: A possible link with Parkinson's disease. (1st November 2017)

• Record Type: Journal Article
• Authors: Abbaoui, Abdellatif; Chatoui, Hicham; El Hiba, Omar; Gamrani, Halima
• Is Part Of: Neuroscience letters. Volume 660(2017)
• Page Start: 103
• Page End: 108
• Publication Date: 2017-11-01
• Subjects: Curcumin -- Copper neurotoxicity -- Midbrain -- Dopamine -- Locomotion -- Wistar rat; Neurology -- Periodicals; Neurology -- Periodicals; Research -- Periodicals; Neurologie -- Périodiques; Neuroanatomie -- Périodiques; Neuropharmacologie -- Périodiques; Neurophysiologie -- Périodiques; Neurology; Periodicals; Electronic journals; 617.48
• DOI: 10.1016/j.neulet.2017.09.032
• Languages: English
• ISSNs: 0304-3940

Abstract

Highlights: Copper (Cu) is a heavy metal that have been wildly involved in several neurodegenerative disorders. The copper toxicity induced alteration of dopaminergic system and could be involved in the neuro-physiopathology of Parkinson disease. Curcumin repair the copper neurotoxicity of dopaminergic system. Abstract: Numerous findings indicate an involvement of heavy metals in the neuropathology of several neurodegenerative disorders, especially Parkinson's disease (PD). Previous studies have demonstrated that Copper (Cu) exhibits a potent neurotoxic effect on dopaminergic neurons and triggers profound neurobehavioral alterations. Curcumin is a major component of Curcuma longa rhizomes and a powerful medicinal plant that exerts many pharmacological effects. However, the neuroprotective action of curcumin on Cu-induced dopaminergic neurotoxicity is yet to be investigated. The aim of the present study was to evaluate the impact of acute Cu-intoxication (10 mg/kg B.W. i.p) for 3 days on the dopaminergic system and locomotor performance as well as the possible therapeutic efficacy of curcumin I (30 mg/kg B.W.). Intoxicated rats showed a significant loss of Tyrosine Hydroxylase (TH) expression within substantia nigra pars compacta (SNc), ventral tegmental area (VTA) and the striatal outputs. This was correlated with a clear decrease in locomotor performance. Critically, curcumin-I co-treatment reversed these changes and showed a noticeable protective effect; both TH expression and locomotor performance was reinstated in intoxicated rats. These results demonstrate altered dopaminergic innervations following Cu intoxication and a new therapeutic potential of curcumin against Cu-induced dopaminergic neurotransmission failure. Curcumin may therefore prevent heavy metal related Parkinsonism.