the protective effect of celecoxib on ca1 hippocampal neurons and oxidative stress in a rat model of parkinson’s disease

Several studies point to an important role of neuroinflammation in parkinson's disease (pd). cognitive and memory impairments have been known in the early stages of pd. in the present study, we examined the effects of celecoxib (clx), a selective inhibitor of cyclooxygenase-2 (cox-2), on hippocampus cell loss, passive avoidance memory and antioxidant status in a rat model of pd. we used the subcutaneous injection of 2.5 mg/kg/48h rotenone (rot) for 4 weeks for induction of pd in a male wistar rat. animals were randomized to 4 groups (n=12): control, sham, pd and pd+clx group that receive celecoxib (20 mg/kg/day) for 4 weeks. passive avoidance memory evaluated. we also determined the protective effect of clx on a number of ca1 neurons in nissl and tunel staining. total antioxidant capacity (tac) and malondialdehyde (mda) a marker of lipid peroxidation in hippocampus assessed. our findings indicated administration of clx increase the passive avoidance memory (p<0.05), and by a decrease in apoptosis caused an increase in viable pyramidal neurons in ca1 hippocampus (p<0.01). on the other hand, clx markedly reduced mda level and increased tac in the hippocampus of the pd model animal (p<0.05). it seems clx with anti-inflammatory and antiapoptotic effect could prevent neurons loss and memory impairment which induced in pd.