Thesis (Ph.D.) - Cairo University - Faculty of Pharmacy - Department of Pharmacology and Toxicology

Escitalopram, a drug of first-choice in the treatment of depression, was recently shown to possess an anti-inflammatory activity. The aim of the present study was to elucidate the effect of escitalopram on peripheral inflammatory cascades in iodoacetamide-induced colitis in normal and ovariectomized rats. Moreover, the involvement of Ü-7 nicotinic acetylcholine receptor in mediating the anti-colitic effect of escitalopram was examined using a nicotinic receptor antagonist methyllycaconitine citrate. Colitis was induced by intracolonic instillation of iodoacetamide. Escitalopram (10 mg/kg) was given once daily for one week. Treatment with escitalopram improved colitis as indicated by a decrease in weight loss, colon mass index, ulcerative area and total histology score. Moreover, it reversed iodoacetamide-induced rise in colonic myeloperoxidase activity, tumor necrosis factor-{uF061} level and corticotropin releasing hormone content. Escitalopram was also effective in normalizing the expression of tight junction proteins in colonic tissues. These potential effects of escitalopram were noticed in the presence of methyllycaconitine. The present study revealed the potential anti- inflammatory effect of escitalopram against iodoacetamide-induced colitis in normal and ovariectomized rats

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