Background: Isoflurane can lead to neuron damage to the developing brain, resulting in learning and memory disability. The aim of this study was to investigate the role of miR-142-5p on isoflurane-induced neurological impairment. Methods: The Morris water maze (MWM) test was performed to evaluate spatial learning and memory of rats. The expression level of miR-142-5p was measured using qRT-PCR. MTT assay was used to calculate the viability of hippocampal neuronal cells. The cell apoptosis was analyzed using Flow cytometric assay. Results: Isoflurane treatment led to the increase of neurological function score and escape latency, and the reduction of time spent in the original quadrant in rats. The expression level of miR-142-5p was increased significantly in isoflurane-treated rats. MiR-142-5p downregulation protected against isoflurane-induced neurological impairment, which was reflected by the decrease of neurological function score and escape latency, and the increase of time spent in the original quadrant. In vitro, downregulation of miR-142-5p alleviated isoflurane-induced neuron cell viability inhibition, and relieved isoflurane-induced cell apoptosis. Conclusions: MiR-142-5p downregulation plays a neuroprotective role in protecting against isoflurane-induced neurological impairment through regulating neuron cell viability and apoptosis. It provides a theoretical basis for the investigation of the mechanism underlying the effect on isoflurane-induced neurological impairment.

A number of microRNAs (miRs) have been identified as being involved in the regulation of anesthesia-induced cognitive impairment. The aim of the present study was to investigated the role and potential mechanism of miR-133b in isoflurane-induced learning and memory impairment. An animal model of isoflurane exposure was established using neonatal Sprague-Dawley rats. The rats were trained for Morris water maze (MWM) testing to assess their spatial learning and memory ability. Reverse transcription-quantitative polymerase chain reaction was used for the measurement of miR-133b expression in hippocampal tissues and primary hippocampal neuron cultures. Cell viability was assessed using a Cell Counting Kit-8 assay, and flow cytometric analysis was used to determine the rate of apoptosis. The MWM test results indicated that during the training period, the time required to locate the platform was significantly increased for rats exposed to isoflurane, and this increased time was reduced by the overexpression of miR-133b. The results of a probe trial indicated that isoflurane exposure increased escape latency and decreased the time spent in the platform area for isoflurane-treated rats; however, these effects were reversed by the injection of miR-133b agomir. The in vitro experiments demonstrated that the overexpression of miR-133b attenuated the reduction of neuronal cell viability induced by isoflurane, and inhibited the isoflurane-induced apoptosis of hippocampal neurons. In conclusion, the present study revealed that the overexpression of miR-133b attenuated isoflurane-induced learning and memory impairment in rats. Furthermore, miR-133b overexpression promoted the viability of hippocampal neurons and their resistance to apoptosis when exposed to isoflurane.