the effects of celecoxib on rotenone-induced rat model of parkinson’s disease: suppression of neuroinflammation and oxidative stress-mediated apoptosis

Background: parkinson’s disease (pd) isoneof themostcommonneurodegenerative movement-related disturbance characterized by the degeneration of dopaminergic neurons with uncertain underlying mechanisms, which can be modeled by the rotenone (rot). neuroinflammation and oxidative stress (os) are the most possible hypotheses to create this condition. objectives: the aim of this study was to evaluate the effects of celecoxib (clx) on rot-induced rat model of pd. to this aim, the suppression of neuroinflammation and oxidative stress-mediated apoptosis was surveyed. methods: in this experimental study, thirty-two male sprague-dawley rats randomly classified into 4 groups (n = 8 rats/group) in the following order: control, sham, pd (2.5 mg/kg/48 hours rot subcutaneously), clx + pd (20 mg/kg/24 daily orally clx + 2.5 mg/kg/48 hours rot). after 28 days of the experiment, the rats were sacrificed and their brain was removed. then histological (nissl staining) and biochemical assessments (total antioxidant capacity (tac) were carried out and malondialdehyde (mda) levels were measured. the data were analyzed by anova test. results: the biochemical assessments showed tac was significantly increased in clx + pd group compared with pd group, whereas mda was decreased in clx + pd group compared with pd group (p < 0.01). we found a significant decrease in the number of dopaminergic cells in substantia nigra pars compacta (snc) in pd group (p < 0.001), and treatment with clx markedly increased dopaminergic neurons in clx + pd compare to pd group (p < 0.01). conclusions: the findings of this study revealed that clx treatment can effectively improve the antioxidant defense system and attenuates striatum insults on rot-induced rat model of pd. these findings suggest that clx plays a neuroprotective role in the inhibition of oxidative stress and neuroinflammation.