Grishma Patel, Sunita Goswami*
L. M. College of Pharmacy, Ahmedabad, Gujarat, India
*Address for corresponding Author
Ms. Sunita Goswami
L. M. College of Pharmacy, Ahmedabad, Gujarat, India
Abstract
Background: Chronic mild stress (CMS) induces behavioral changes, oxidative-stress and neuroinflammation. CMS mimics the clinical aspects of anxiety and depression. Current antidepressant drugs have slow onset of action, low response rates and problem of drug resistance. Therefore, there is a scope of new therapy for the treatment of psychiatry disorders. Objectives: The present study is aimed to assess the efficacy of ibuprofen and etoricoxib in CMS model using mice and to explore the possible mechanism for the same. Materials and Methods: Animals were exposed to CMS procedure for 28 days. The mice were daily treated with ibuprofen (15mg/kg p.o.), etoricoxib (5mg/kg p.o.) and venlafaxine (10 mg/kg p.o., reference standard) for 14 days, 2 h before exposure to stress procedure. The behavioural consequence of depression was measured in terms of immobility time, locomotor activity, anxiety level by elevated plus maze model and sucrose preference test respectively. The biochemical estimations included serum corticosterone, reduced glutathione (GSH), neurotransmitter estimation and quinolinic acid level measurement, serotonin, noradrenaline, and dopamine. Results: The animals treated with ibuprofen, etoricoxib and concomitant treatment of both ibuprofen and venlafaxine showed significant increase in sucrose preference and locomotor activity along with decrease in immobility time, corticosterone level, adrenal gland weight, and quinolinic acid levels. Further, they also significantly raised brain neurotransmitters levels viz. serotonin, nor-adrenaline, and dopamine. Conclusion: The anti-depressant action of these drugs can be attributed to improvement of brain neurotransmitter levels, reduction in the corticosterone and quinolinic acid leading to neuroprotection in the CNS.
Keywords: Ibuprofen, etoricoxib, neuro-inflammation, NSAIDs
