Akademik Veri Yönetim Sistemi
International Journal of Pharmacology, cilt.18, sa.1, ss.44-52, 2022 (SCI-Expanded)
Background and Objective: It is known that nimesulide reduces the toxic effects of Non-Steroidal Anti-Inflammatory Drugs (NSAID),
eliminating their inhibitory effects on cyclooxygenase-1 (COX-1) enzyme. COX-1 enzyme inhibition is thought to be responsible
for aspirin ototoxicity therefore current study aimed to investigate the effect of nimesulide on aspirin ototoxicity in rats.
Materials and Methods: Nimesulide 100 mg kgG1
orally was administered to the nimesulide+aspirin group (NASA) and the same volume
of distilled water as solvent was administered to the aspirin group (ASA) and the healthy (HG) group. Aspirin at a dose of 1000 mg kgG1
was administered orally to the NASA and ASA group one hour after the administration of nimesulide and solvent. This procedure was
repeated once a day for 7 days. Then, the animals were euthanized with a high dose of anaesthesia (50 mg kgG1
thiopental sodium) and
their cochlea and cochlear nerve tissues were removed. Results: Malondialdehyde (MDA) level was significantly higher and total
glutathione (tGSH) and cyclooxygenase-1 COX-1 levels were significantly lower in the ASA group in which prominent histopathological
damage was found in the cochlea and cochlear nerve, compared to the HG and NASA group. The COX-2 level was found to be almost
the same in all the groups. This indicates that aspirin reduces the COX-1 and tGSH levels and increases the MDA level, causing ototoxicity.
Conclusion: Aspirin significantly decreased the COX-1 activity in the cochlea and cochlear nerve tissue, compared to the healthy and
nimesulide group. Current study concluded that the co-administration of nimesulide and aspirin will increase the therapeutic effect of
aspirin and reduces its side-effects.