Background Recent studies showed that aminoglycosides destroyed the cochlear cells and induced ototoxicity byproducing reactive oxygen species,including free radicals in the mitochondria,damaging the membrane of mitochondriaand resulting in apoptotic cell death.BCI-XL is a well characterized anti-apoptotic member of the Bcl-2 family.The aim ofthis study was to determine the potential cochlear protective effect of Bcl-XL as a therapeutic agent in the murine model ofaminoglycoside ototoxicity.Methods Serotype 2 of adeno-associated virus(AAV2)as a vector encoding the mouse BCI-XL gene was injected intomice cochleae prior to injection of kanamycin.Bcl-X_L expression in vitro and in vivo was examined with Western blottingand immunohistochemistry separately.Cochlear dissection and auditory’ steady state responses were checked toevaluate the cochlear structure and function.Results The animals in the AAV2-Bcl-xL/kanamycin group displayed better auditory steady state responses hearingthresholds and cochlear structure than those in the artificial perilymph/kanamycin or AAV2-enhanced humanized greenfluorescent protein/kanamycin control group at all tested frequencies.The auditory steady state responses hearingthresholds and cochlear structure in the inoculated side were better than that in the contralateral side.Conclusions AAV2-Bcl-X_L afforded significant preservation of the cochlear hair cells against otetoxic insults andprotected the cochlear function.AAV2-mediated Bcl-X_L might be an approach with respect to potential therapeuticapplication in the cochlear degeneration. Background Recent studies showed that aminoglycosides destroyed the cochlear cells and induced ototoxicity byproducing reactive oxygen species, including free radicals in the mitochondria, damaging the membrane of mitochondria and resulting in apoptotic cell death. BCI-XL is a well-characterized anti-apoptotic member of the Bcl -2 family. The aim of this study was to determine the potential cochlear protective effect of Bcl-XL as a therapeutic agent in the murine model of aminoglycoside ototoxicity. Methods Serotype 2 of adeno-associated virus (AAV2) as a vector encoding the mouse BCI- XL gene was injected intomice cochleae prior to injection of kanamycin.Bcl-X_L expression in vitro and in vivo was examined with Western blotting and immunohistochemistry separately. Cochlear dissection and auditory ’steady state responses were checked to evaluate the cochlear structure and function. Results The animals in the AAV2-Bcl-xL / kanamycin group displayed better auditory steady state response hearingthresholds and cochlear structure than those in the artificial perilymph / kanamycin or AAV2-enhanced humanized green fluorescenceious protein / kanamycin control group at all tested frequencies. auditory steady state response hearingthresholds and cochlear structure in the inoculated side were better than that in the contralateral side. AAV2-Bcl-X_L afforded significant for the cochlear hair cells against otetoxic insults and protected the cochlear function. AAV2-mediated Bcl-X_L might be an approach with respect to potential therapeuticapplication in the cochlear degeneration.