The role of long non-coding RNA SNHG12 in neuroprotection following cerebral ischemic injury.

As one of the major causes of mortality and disability worldwide, ischemic stroke has never been received enough attention. Following ischemia/reperfusion injury, long non-coding RNAs have been extensively found to be involved into inflammatory responses, microvascular endothelial cell death, and angiogenesis in the brain. The small nucleolar RNA host gene 12 was found to be significantly increased following transient middle cerebral artery occlusion. However, the effect and underlying mechanism of small nucleolar RNA host gene 12 in ischemic stroke remain to be explored. We established an oxygen-glucose deprivation/reoxygen in primary neurons model to mimic ischemic stroke. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide assay and lactate dehydrogenase assay were used to prove that knockdown small nucleolar RNA host gene 12 reduced cell viability after oxygen-glucose deprivation/reoxygen treatment. And the western blot showed that knockdown small nucleolar RNA host gene 12 aggravated the oxygen-glucose deprivation/reoxygen-induced apoptosis. What's more, the pro-inflammatory cytokine level was increased in small nucleolar RNA host gene 12 knockdown primary neurons. Mechanistically, the specific distribution of small nucleolar RNA host gene 12 in primary neurons was detected by fluorescence in situ hybridisation. Additionally, we demonstrate small nucleolar RNA host gene 12 attenuates oxygen-glucose deprivation/reoxygen injury through activating Akt signaling pathway. Therefore, the small nucleolar RNA host gene 12 may be the new potential therapeutic target for the alleviation of cerebral ischemic injury.