Abstract: Objective To investigate the effect of miR-338-3p on ischemic injury of neurons after oxgen glucose deprivation(OGD)/reoxgenation(R). Methods In vivo model of middle cerebral artery occlusion(MCAO) was developed in mice and in vitro model of oxygen glucose deprivation(OGD) was developed with in cortical neurons. Using Western blot to detect cPKCγ protein levels in peri-infarct cortex of mice(n=5) with 1 h MCAO/R 24,48 and 72 h and in neurons(n=5) with 1 h OGD/R 0,6,12 and 24 h; using quantitative RT-qPCR to detect miR-338-3p and cPKCγ mRNA; using bioinformatics to detect the binding sites of cPKCγ 3′UTR and miR-338-3P. Using MTT and LDH methods to detect the survival rate and apoptosis rate of nurons(n=6); using immunofluorescence and HCA to detect the expression of caspase-3 in neurons(n=5). Results cPKCγ protein and mRNA significantly increased in mice with 1 h MCAO/R 24,48 and 72h and in neurons with 1 h OGD/R 0,6,12 and 24 h(P＜0.001); cPKCγ 3′UTR had one miR-338-3p binding site; the miR-338-3p mRNA level showed an opposite trend to that of cPKCγ mRNA level; after over-expression miR-338-3p, the survival rate decreased(P＜0.001) and the apoptosis rate increased(P＜0.001) and the mean fluorescence intensity of caspase-3 increased(P＜0.001) in neurons after 1 h OGD/R 24 h. After inhibition miR-338-3p, the survival rate increased(P＜0.001), the apoptosis rate decreased(P＜0.001) and the mean fluorescence intensity of caspase-3 decreased(P＜0.001) in neurons after 1 h OGD/R 24 h. Conclusions miR-338-3p enhances the survival rate and reduces apoptosis rate of ischemic neurons by negatively regulation of cPKCγ and so to alleviate the injury of ischemic neurons.

Key words: miR-338-3p, cPKCγ, middle cerebral artery occlusion(MCAO), oxygen glucose deprivation(OGD)