Autophagy, a self-digestion intracellular catabolic process, plays a crucial role in cellular homeostasis. Our previous studies demonstrated that noise at 110-dB sound pressure level (SPL) produced permanent hearing impairment. In the present study, we prepared an animal model of permanent hearing loss and sought to determine whether rapamycin (autophagy activator) have preventive effect on noise-induced hearing loss in the model mice. To determine the activation of autophagy following noise exposure, we evaluated the expression of LC3-II (LC3 = LC3-II/LC3-I, autophagy marker) in the cochlea after a 1-h exposure to noise at 110 dB SPL. Immunoblot analysis revealed that noise exposure produced a dramatic increase in the LC3-II level of the cochlea at 1-h post-exposure.  Moreover, rapamycin significantly alleviated hearing impairment induced by exposure to noise at 110-dB SPL.  In addition, immunohistochemistry analysis revealed that rapamycin was effective in enhancing expression of LC3 in the cochlear lateral wall. Taken together, our data suggest that autophagy activator is a candidate of preventive drugs for sensorineural hearing loss.