Abstract
Cerebral ischemic stroke is a major cause of adult morbidity and mortality worldwide. Several long non-coding RNAs (lncRNAs) have been reported to participate in cerebral ischemia/reperfusion injury (IRI). However, to the best of our knowledge, the role of lncRNA AK139328 in cerebral ischemic stroke remains poorly understood. The present study aimed to determine the expression and function of lncRNA AK139328 in the progression of IRI. PC12 cells were injured by oxygen glucose deprivation/reoxygenation (OGD/R) to establish an in vitro ischemic stroke model. An MTT assay was performed to determine cell viability. Reverse transcription-quantitative PCR was used to analyze the expression levels of AK139328 and Netrin-1 in blood samples from patients who had suffered a cerebral ischemic stroke and healthy individuals or OGD/R PC12 cells. ELISAs were used to determine the levels of inflammatory cytokines. In addition, oxidative stress levels and the levels of cell apoptosis were evaluated by reactive oxygen species (ROS) kits, flow cytometry and western blotting. Immunofluorescence staining was used for the detection of cell neurite outgrowth. The results of the present study revealed that AK139328 expression levels were upregulated in patients who had suffered a cerebral ischemic stroke and in PC12 cells following stimulation with OGD/R. The knockdown of AK139328 alleviated OGD/R-induced decreases in cell viability, downregulation in Netrin-1 expression and increases in inflammatory cytokines levels, including TNF-α, IL-1β and IL-6. Moreover, AK139328 silencing suppressed oxidative stress and cell apoptosis in OGD/R-treated PC12 cells. Furthermore, the expression levels of microtubule associated protein 2 and growth associated protein 43 in OGD/R-injured PC12 cells were upregulated following the knockdown of AK139328 expression. In conclusion, these findings suggested that the knockdown of AK139328 expression may protect PC12 cells against OGD/R injury by regulating inflammatory responses, oxidative stress and cell apoptosis. The data suggested a potential therapeutic target for the diagnosis and treatment of cerebral ischemic stroke.