Effect of Cyclooxygenase-2 inhibition on rigidity of animal model of Parkinson's disease

• Main Authors: Fathi Moghaddam, Shafiee Ardestani, Hemmati, Nazari
• Format: Article
• Language: fas
• Published: Tehran University of Medical Sciences 2008-08-01
• Series: Tehran University Medical Journal
• Subjects: Parkinson’s disease; cyclooxygenase-2; celecoxib; aspirin
• Online Access: http://journals.tums.ac.ir/PdfMed.aspx?pdf_med=/upload_files/pdf/10424.pdf&manuscript_id=10424

"nBackground: Parkinson's disease (PD) is a degenerative neurodopaminergic disease in nigrostriatum pathway of animals and human, the resultant loss of nerve terminals accompanied by dopamine-glutamate and other related neurotransmitters-imbalances in this pathway are responsible for most of the movement abnormalities. Increasing evidence suggests that an inflammatory reaction accompanies the pathological processes caused by Cyclooxygenase-2 (COX-2) seen in many neurodegenerative disorders, including PD. These findings have not indicated any evidence based on the effect of selective and non selective COX-2 inhibitors on the rigidity of PD."n"nMethods: The rats left substantia nigra pars compacta (SNc) was destroyed using the electrical lesion thus PD model was created. Then oral aspirin and celecoxib (200, 400 mg/kg) were administrated to parkinsonian rats acutely and then the rigidity was evaluated using Murprogo's Method."n"nResults: Both compounds were able to decrease the rigidity of parkinsonian rats (p<0.05) respectively but selective cox-2 inhibitor (celecoxib) was found more effective and potent than that of non selective cox-2 inhibitor (aspirin)."n"nConclusion: The findings suggest that COX-2 inhibition decreases the rigidity of PD in the animal model. Therefore, as results of the study COX-2 inhibition was shown good evidence based on the use of aspirin and celecoxib and PD affiliated rigidity improvement that this can be beneficial and interest for neuroscientists. These findings are additional pharmacological and medicinal information to further assess of non steroidal anti inflammatory drugs (NSAIDs) as alternative therapeutic agents for PD affiliated rigidity treatment. Further experiments seem to be necessary to complete this research such as investigation the effects of NSAIDs on the striatum neurotransmission pathway