Objective To investigate the effect of oleuropein on cochlear tissue damage in noise-induced hearing loss (NIHL) rats by regulating the proline-rich Akt substrate of 40 kDa (PRAS40)/mammalian target of rapamycin complex 1 (mTORC1) signaling pathway. Methods A total of 48 rats were selected, 12 rats were randomly regarded as the control group, and the remaining rats were used to construct NIHL rat model using white noise. Subsequently, the NIHL model rats were randomly grouped into model group, oleuropein group, and oleuropein+NV-5138 group, each group consisted of 12 rats and was given corresponding intervention for 7 days. The threshold of auditory brainstem response (ABR) was evaluated. Hematoxylin-eosin staining was applied to detect pathological damage in cochlear tissue. The apoptosis of cochlear tissue was detected by TdT-mediated dUTP nick end labeling staining. The sequences of hair cells in the cochlear basement membrane were observed by confocal microscopy. Western blot was applied to detect the expression of phosphorylated PRAS40 (p-PRAS40), PRAS40, phosphorylated mTORC1 (p-mTORC1), mTORC1, and B-lymphoblastoma-2 related X protein (Bax) in rat cochlear tissue. Results Compared with control group, the number of spiral ganglion cells in the cochlear tissue in the model group was significantly reduced, the morphology was abnormal, the structure of basal membrane hair cells was severely damaged, no obvious boundary could be seen, the cell arrangement was not orderly, the ABR threshold, the number of apoptotic cells in cochlear tissue, the p-mTORC1/mTORC1 protein ratio, and the expression of Bax protein were significantly increased, the p-PRAS40/PRAS40 protein ratio was significantly decreased (P<0.05). Compared with model group, the number of spiral ganglion cells in the cochlear tissue of oleuropein group increased and their shape recovered, the damage of basement membrane hair cells was reduced, the cell arrangement gradually returned to normal, the boundary became clear, and the ABR threshold, the number of apoptotic cells in cochlear tissue, the p-mTORC1/mTORC1 protein ratio and the expression of Bax protein were significantly decreased, and the p-PRAS40/PRAS40 protein ratio was significantly increased (P<0.05). After the intervention of NV-5138, the improvement effects of oleuropein on the pathological injury of cochlear tissue, basal membrane hair cell sequence and the above indexes in NIHL rats were weakened (P<0.05). Conclusion Oleuropein may promote PRAS40 phosphorylation and inhibit mTORC1 phosphorylation by regulating PRAS40/mTORC1 signaling pathway, thereby alleviating cochlear tissue injury in NIHL rats.