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Electroacupuncture (EA), a modern form of acupuncture therapy, has been widely used for the treatment of ischaemic brain injury. However, the molecular mechanism by which EA improves ischaemic brain injury remains unclear. In the current study, middle cerebral artery occlusion (MCAO) rats were treated with EA. The infarct volumes and apoptosis of neurocytes were assessed to determine the therapeutic effect of EA. The differentially expressed miRNAs between the control, MCAO and MCAO treated with EA groups were detected by high-throughput sequencing. The results indicated that EA treatment decreased neurocyte apoptosis and ischaemic infarct volume. Between the three groups, miR-34, miR-235 and miR-275 were found to be significantly different. Furthermore, the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway data suggest that the Wnt pathway may play an important role in ischaemic brain injury and in the treatment of EA. Our data documented that miR-34 was obviously increased in the MCAO group, while EA treatment decreased miR-34 expression. WNT1 was the target of miR-34 and was confirmed by a luciferase reporter assay. A previous study suggested that the Wnt pathway mediates autophagy in EA-pretreated MCAO mice. Our data further confirmed that EA treatment after MCAO also alleviated autophagy in the MCAO group. Our results suggest that EA treatment alleviates ischaemic brain injury by inhibiting autophagy through the miR-34/Wnt pathway., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Brain ischaemia, which can cause severe nerve injury, is a global health challenge. Long non-coding RNA (lncRNA) growth-arrest specific 5 (Gas5) has been documented to exert tumour suppressive effects in several cancers. However, its role in cerebrovascular disease still requires further investigation. Therefore, in this study, we focused on the role of lncRNA regulatory signalling related to lncRNA Gas5 in ischaemic brain injury. Middle cerebral artery occlusion (MCAO) was employed as a model of ischaemic brain injury in rats. The expression of lncRNA Gas5 and microRNA-21 (miR-21) was altered in neurons to elucidate their effects in ischaemic brain injury and to identify the interactions among lncRNA Gas5, miR-21 and Pten. The neuronal survival rate, apoptosis and the expression of phosphatidyl inositol 3-kinase (PI3K)/Akt signalling pathway-related genes were also evaluated in vitro to determine the effects of lncRNA Gas5. In the brains of rats subjected to MCAO, the expression of lncRNA Gas5 and Pten was upregulated, while miR-21 was downregulated. LncRNA Gas5 inhibited miR-21 expression, leading to elevated levels of Pten. In vitro experiments revealed that lncRNA Gas5 depletion and miR-21 elevation resulted in the suppression of neuronal apoptosis, thus promoting neuronal survival via the PI3K/Akt signalling pathway. These findings demonstrate that lncRNA Gas5 increases miR-21 and activates Pten, contributing to the development of ischaemic brain injury, supporting the silencing of lncRNA Gas5 as a possible therapeutic target for the treatment of ischaemic brain injury., (Copyright © 2020. Published by Elsevier Ltd.)