Role of microRNA-134 in the neuroprotective effects of propofol against oxygen-glucose deprivation and related mechanisms.

This study is to investigate the effects of propofol on primary hippocampal neurons under oxygen-glucose deprivation (OGD) condition and related mechanisms. The apoptotic process was detected with flow cytometry, and the cell viability was assessed with CCK-8 assay. The expression levels of microRNA (miRNA)-134 were detected with quantitative real-time PCR. Protein expression levels were detected by Western blot analysis. Dual-luciferase reporter assay was also performed to confirm the prediction of the target genes of miRNA-134. Our results from flow cytometry showed that the apoptosis rate was significantly increased in the primary hippocampal neurons under OGD condition. However, the treatments of propofol (25, 50, 100, and 150 µmol/L) suppressed the apoptotic process. Moreover, propofol restored the declined cell viability in the primary hippocampal neurons under OGD condition. In addition, compared with the OGD model group, the Bcl-2/Bax ratios were significantly elevated in the propofol-treated groups, indicating the protective effects of propofol against cellular apoptosis. Quantitative real-time PCR showed that propofol reduced the expression levels of miRNA-134 in the primary hippocampal neurons under OGD condition. Bioinformatics analysis revealed that BDNF might be a target of miRNA-134. The treatment of antago-miRNA-134 significantly down-regulated the expression level of BDNF. In line with this, dual-luciferase reporter assay suggested that miRNA-134 targeted BDNF in the 3'-TUR. Under OGD condition, propofol could down-regulate miRNA-134, and subsequently modulate the expression of BDNF, to exert neuroprotective effects.