Electroacupuncture (EA) pretreatment has been reported to induce tolerance against cerebral ischemia/reperfusion (I/R) injury; however, the mechanisms underlying the beneficial effects of EA remain to be elucidated. Increasing evidence has suggested that excess activation of autophagy is important in I/R injury. The present study aimed to investigate the hypothesis that EA pretreatment‑induced tolerance to cerebral I/R injury was mediated by inhibition of the autophagy pathway. Rats were treated with EA at the acupoint 'Baihui (GV20)' 30 min/day, for five consecutive days prior to the induction of focal cerebral ischemia for 120 min by middle cerebral artery occlusion. Levels of autophagy, cerebral apoptosis, infarct volumes, brain water content and motor deficit were evaluated 12 h following I/R. The autophagy inducer rapamycin was used to investigate the role of autophagy in mediating neuroprotective effects. The results showed that the number of autophagosomes and the expression of the marker proteins of autophagy, including microtubule‑associated protein 1A light chain 3 (LC3)‑II and Beclin 1 were significantly increased 12 h post‑I/R. EA pretreatment decreased the expression of autophagy markers and the number of autophagosomes in the ischemic cortex. In addition, EA pretreatment inhibited neuronal apoptosis, reduced infarct volume and water content, as well as improved neurological outcome of rats following I/R. Furthermore, the reduced expression of LC3‑II and Beclin 1 and the neuroprotective effects were reversed by the autophagy inducer rapamycin. In conclusion, the results of the present study demonstrated that EA pretreatment protected the brain against I/R injury via inhibition of the autophagy process.

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The present study aimed to investigate the function of micro (mi)RNA-153 against isoflurane-induced neurotoxicity and its mechanism. In isoflurane-induced mice, miRNA-153 expression was downregulated compared with in the control group. Downregulation of miRNA-153 induced neurocyte apoptosis, reduced cell growth and promoted oxidative stress in an in vitro model. Overexpression of miRNA-153 reduced oxidative stress, promoted cell growth and inhibited neurocyte apoptosis within an in vitro model. Downregulation of miRNA-153 suppressed nuclear erythroid-2 related factor 2 (Nrf2)/antioxidant response element (ARE) signaling pathway, which was induced via the overexpression of miRNA-153 in vitro . The Nrf2 agonist, dimethyl fumarate (2.5 µM), induced the Nrf2/ARE signaling pathway and reduced oxidative stress to induce neurocyte apoptosis in vitro following treatment with anti-miRNA-153. The results of the present study suggested the function of miRNA-153 against neurotoxicity via Nrf2/ARE-mediated cytoprotection.