Abstract: To study the expression of iNOS in amikacin(Amk)-induced spiral ganglion neuron(SGN) apoptosis in the rat cochlea and the protection of (-)-epigallocatechin-3-gallate(EGCG). MethodsAnimals were divided into three groups: one group serving as the saline control group, one group receiving Amk at 450mg/kg once a day for 14 days, and one group receiving Amk plus EGCG at 50mg/kg once a day for 14 days. Following deep anesthesia, the animals were half-body perfused intracardially with 4% paraformaldehyde (PFD), and the bullas were harvested, fixed in PFD, and decalcified in ethylenediamine tetraacetic acid (EDTA). After decalcification, the cochlea were embedded in paraffin, and subsequently cut in a paramodiolar plane. Immunohistochemical changes were observed by detecting with iNOS. ResultsThe negative immunohistochemical reaction for iNOS-staining was found in the SGNs in the saline control group, and the positive reaction was found in the cytoplasm of part of the SGNs of the group receiving Amk. However, positive staining could hardly be detected in the group receiving Amk plus EGCG. Image analysis showed that the expression of iNOS was significantly up-regulated in the group receiving Amk, but this up-regulation was significantly suppressed by EGCG. ConclusionsiNOS was involved in Amkinduced oxidative damages to the SGN in the rat cochlea. EGCG effectively attenuated Amk-induced ototoxicity and suppressed Amk-induced SGN apoptosis by the influence on the expression of iNOS.

Key words: Amikacin, Spiral ganglion neuron, (-)-epigallocatechin-3-gallate, Inducible nitric oxide synthase