الفهرس 
The inflammatory hypothesis of depressionOnly 14 pages are availabe for public view
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Abstract
The cytokine hypothesis of depression suggests that inflammatory processes and immune interactions are involved in the pathogenesis of major depression. PG and NO are important inflammatory mediators that are increased in depression and decreased by NSAIDs. The aim of the present work is to explore a possible antidepressant action of ibuprofen, possibly mediated through inhibition of PG and NO synthesis in the model of BCG induced depressive like behaviour.
Locomotor activity was not affected in any of the tested groups with the exception of the rofecoxib treated group. BCG inoculation in the present study resulted in a depressive like behaviour manifested as an increase in the total immobility time in the FST and TST and an increase in the brain levels of both NO and PGE2 with intense immunoreactivity for nNOS, iNOS, COX-1 & COX-2 in immunohistochemistry of mice hippocampus. Ibuprofen exhibited an antidepressant effect comparable to that of fluoxetine in both the FST and TST. It also decreased the brain levels of both NO and PGE2 with decrease in intensity immunoreactivity for COX-1 and iNOS, and to a lesser extent COX-2 and nNOS in areas CA1 and CA3 of hippocampus. Fluoxetine as well, decreased the brain levels of both NO and PGE2. Addition of the NO donor L-arginine reversed the behavioural and biochemical effect induced by both ibuprofen and L-arginine.
It can be concluded that in the murine model of chronic immune activation and depressive like behaviour induced by BCG inoculation, ibuprofen exhibits an antidepressant effect comparable to that of fluoxetine. This antidepressant effect, is mediated at least in part through inhibiting NO and PGE2 synthesis.