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MicroRNAs plays important role in cerebral ischemia-reperfusion (CIR). However, the role of miR-26b-5p in CIR injury remains unclear. PC12 cells were treated with oxygen-glucose deprivation (OGD) for 0 h, 2 h, 4 h, 6 h, and then reoxygenated for 24 h to construct an in vitro I/R model. Then, miR-26b-5p mimic, small interfering RNA of KLF10 and KLF10 overexpression plasmid were transfected into cells respectively for mechanism study. Our results showed that miR-26b-5p was downregulated in OGD/R-induced PC12 cells. After overexpression of miR-26b-5p, cell proliferation ability was enhanced, apoptosis, ROS and inflammatory mediators were inhibited. Bioinformatics analysis indicated that miR-26b-5p was directly bound to the 3’ UTR of KLF10, and downregulated the expression of KLF10. KLF10 was upregulated in OGD/R cells, and transfection with si-KLF10 promoted cell proliferation and reduced apoptosis, NO concentration and inflammatory factor secretion. Moreover, pcDNA-KLF10 reversed the inhibitory effects of miR-26b-5p mimic on apoptosis, NO content and inflammatory factor secretion, as well as the downregulation of N-myc and PTEN expression. Meanwhile, I/R rat models were constructed and divided into sham operation group (femoral artery isolation only), model group (middle cerebral artery occlusion model of rats was prepared by thread embolization), treatment group (200 µL of miR-26b-5p mimic was injected into the brain of model rats). We observed that the infarct size of brain tissue was reduced, KLF10 expression was downregulated, and apoptosis and inflammatory response were reduced. These results suggest that miR-26b-5p had protective effects on CIRI and it may be a potential treatment target.

MicroRNA-26b-5p alleviates cerebral ischemia-reperfusion injury in rats via inhibiting the N-myc/PTEN axis by downregulating KLF10 expression