Electroacupuncture Promotes Autophagy by Regulating the AKT/mTOR Signaling Pathway in Temporal Lobe Epilepsy.

Temporal lobe epilepsy (TLE) is a complex neurological disease, and its occurrence and development are closely related to the autophagy signaling pathway. However, the mechanism by which electroacupuncture (EA) affects the regulation of autophagy has not been fully elucidated. TLE gene chip dataset GSE27166 and data from rats without epilepsy (n = 6) and rats with epilepsy (n = 6) were downloaded from Gene Expression Omnibus. The differentially expressed genes (DEGs) in the TLE and control groups were identified with the online tool GEO2R. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) databases were used to analyse the functional and pathway enrichment of genes in the most important modules. A rat model of TLE induced by lithium-pilocarpine treatment was established. EA treatment at DU20 and DU14 in TLE rats was performed for 2 weeks. Neuronal regeneration was determined using immunofluorescence staining. The protein levels of AKT/mTOR signaling pathway and autophagy markers were detected through western blotting and immunohistochemistry. This study identified 1837 DEGs, including 798 upregulated genes and 1039 downregulated genes. GO enrichment and KEGG analyses were performed on DEGs and revealed functional enrichment mainly in the mTOR signaling pathway and autophagy-animal. Furthermore, the number of mature neurons was significantly increased upon coexpressing BrdU/NeuN in TLE rats treated with EA. Western blotting and immunohistochemistry results showed significantly decreased levels of the phosphorylated-AKT and p-mTOR in the hippocampal CA3 and DG regions of TLE rats with EA treatment. And increased p-ULK1/ULK1, LC3-II/LC3-I and p62 levels in TLE rats with EA stimulation. Therefore, this study suggested that EA promoted autophagy in hippocampal neurons during the onset of epilepsy by regulating the AKT/mTOR signaling pathway to treat epilepsy.

Protective effects of Acanthopanax polysaccharides on cerebral ischemia-reperfusion injury and its mechanisms.

A kind of Acanthopanax polysaccharides extracted from the root of Acanthioanax senticosus was named CASPs. The protective effect of CASPs on the cerebral ischemia-reperfusion injury was observed and the underlying mechanism was explored. Wistar male rats were randomly divided into six groups, namely, sham-operated group, model group, nimodipine group (15 mg/kg/day) and CASPs groups (50, 100 and 200 mg/kg/day). The suture method was used to embolize the middle cerebral artery to establish a rat cerebral ischemia-reperfusion injury model. On day 15 before the surgery, the intragastric administration of agents started once daily. The results confirmed that the CASPs could improve the symptoms of rats with the cerebral ischemia-reperfusion injury, and reduce the brain infarct volume and brain water content. In addition, CASPs could elevate SOD and GSH-Px activities and IL-10 levels, and reduce MDA, IL-1ß and TNF-α levels in the brain tissue of rats with the cerebral ischemia-reperfusion injury. The results indicate that CASPs can play a certain protective role in the cerebral ischemia-reperfusion injury, and the protective effect may be related to the improvement of CASPs on the antioxidant capacity of brain tissue and the inhibition of overproduction of inflammatory cytokines.