Long non-coding RNA H19 inhibition ameliorates oxygen-glucose deprivation-induced cell apoptosis and inflammatory cytokine expression by regulating the microRNA-29b/SIRT1/PGC-1α axis

As one of the earliest discovered long non-coding (lnc)RNAs, lncRNA H19 imprinted maternally expressed transcript (H19) participates in regulating ischemic stroke. The present study aimed to investigate the combined roles of lncRNA H19, microRNA (miR)-29b, silent mating-type information regulation 2 homolog 1 (SIRT1) and peroxisome proliferator-activated receptor-g co-activator-1 alpha (PGC-1 alpha) following ischemic stroke. lncRNA H19 expression levels in the middle cerebral artery occlusion (MCAO) mouse model and HT22 cells subjected to oxygen-glucose deprivation (OGD) were detected via reverse transcription-quantitative PCR (RT-qPCR). H19 small interfering RNA was used to knockdown H19 expression. Following OGD treatment, MTT, flow cytometry, ELISA, RT-qPCR and western blotting assays were performed to assess cell proliferation, cell apoptosis, inflammatory cytokine concentrations, and lncRNA H19, miR-29b, SIRT1, PGC-1 alpha expression levels, respectively. In the present study, MCAO model mice and OGD-treated cells displayed significantly increased lncRNA H19 expression levels compared with sham mice and control cells, respectively. lncRNA H19 knockdown ameliorated OGD-induced cell apoptosis and increases in inflammatory cytokine concentrations. Furthermore, lncRNA H19 knockdown also attenuated OGD-mediated downregulation of miR-29b, SIRT1 and PGC-1 alpha expression levels. Collectively, the results of the present study demonstrated that lncRNA H19 knockdown ameliorated OGD-induced cell apoptosis and increases in inflammatory cytokine concentrations by regulating miR-29b, SIRT1 and PGC-1 alpha expression levels, which suggested the potential role of lncRNA H19 in ischemic stroke.