Objective To investigate the protective effect and biological mechanism of miR-214 on neuronal injury induced by propofol anesthesia, and elucidate the underlying mechanisms of this process. Methods Seven-day-old male Sprague-Dawley rats were randomly divided into four groups (15 rats per group): normal saline (NS), propofol anesthesia thoracotomy exploration ( model), miR-NC and miR-214. With the exception of the NS group, all groups underwent establishment of the propofol anesthesia thoracotomy exploration model. In miR-NC and miR-214 groups, miR-NC-agomir or miR-214-agomir, respectively, were injected into hippocampus before anesthesia. Expression of mTORC1 in the hippocampus was detected by immunofluorescence, apoptosis was detected by TUNEL staining, and expression of miR-214 in hippocampus was analyzed by RT-qPCR. HT22 hippocampal neurons were transfected with an miR-214 inhibitor and mTORC1 inhibitor, and then exposed to propofol. Flow cytometry was used to analyze cell survival, whereas Western blot was used to analyze protein expression of TEFB and C-caspase3. Results Compared with the NS group, miR-214 in the hippocampus of the model group was significantly downregulated (P< 0.05) and apoptosis of hippocampal neurons was significantly increased (P< 0.05). Compared with the model group, apoptosis of hippocampal neurons in the miR-214 group was decreased ( P< 0.05). Bioinformatics prediction indicated the presence of a specific binding site between mTORC1 and miR-214. Compared with the NS group, expression of mTORC1 was increased in the model group ( P<0. 05), and miR-214 treatment significantly reduced expression of mTORC1 (P<0.05). In addition, compared with the NC group, si-mTORC1 transfection significantly reduced the apoptosis rate of HT22 hippocampal neurons exposed to propofol (P< 0.05), increased TFEB expression (P< 0.01), and decreased cleaved caspase 3 ( P< 0. 05). miR-214 inhibitor transfection significantly reversed the protective effect of si-mTORC1 and changes of TFEB and C-caspase3 protein expression induced by si-mTORC1 ( P< 0.05). Conclusions miR-214 attenuates propofol neurotoxicity through the mTORC1-TFEB pathway and improves the survival rate of neurons.