Abstract
Previous clinical studies confirm the presence of inflammatory mediators like tissue necrotic factor alpha (TNF-α) and interleukins-1β in depressive patients are the main cause of depression and the use of non-steroidal anti-inflammatory drugs (NSAIDs) especially cyclo-oxygenase-2 (COX-2) inhibitors are associated with a marked reduction in the symptoms of depression. In our study we investigated the role of diclofenac in ameliorating depression in chlorpromazine (CPZ) induced PD model. Forty Wistar albino rats were divided equally into 4 groups, Rats of group I (control) received only vehicles and had free access to food and water. Rats of groups II, III and IV were treated with chlorpromazine (3mg/kg/day ) via the intraperitoneal route once a day for 21 days. Diclofenac (20mg/kg/day) was given orally to group III and standard drug L-dopa/carbidopa (30mg/kg/day) orally was given to group IV for 21 days. Group II was negative control, and all treated group received 3mg/kg/day i.p CPZ for 21 days. CPZ was administered 30 min before the administration of test drugs, antidepressant effects of diclofenac were examined by using open field activity, cage crossing and forced swimming test. In the open field, diclofenac and standard drug (L-dopa/carbidopa) animals showed significant (P<0.001) improved number of square crossed in 10 minutes, increased grooming period and relatively more time spent in center of open field arena after 10 and 21 days as compared to CPZ group. In cage crossing diclofenac showed highly significant (P<0.001) improved activity of cage crossing after 21 days just similar to standard group (L-dopa/carbidopa), while CPZ significantly showed immobility and depressive behavior. In FST diclofenac was able to restore significantly the immobility time and decrease swimming effort as well as climbing duration induced by CPZ. Taken together, the present work evidenced antidepressant effects of diclofeanc. This may be through inhibiting depressive markers like TNF-α and IL-1β in brain compartments, and possibly nor-adrenergic mechanism could also play a role.
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