Abstract
Ischemic stroke is one of the main causes of physical disability and mortality worldwide. Long non-coding RNAs (lncRNAs) are reported to be dysregulated in various biological progressions and serve important roles in pathological processes of cerebral ischemia. However, their biological actions and potential mechanisms in the progression of ischemic stroke remain unknown. The present study aimed to investigate the functions of LINC00319 on ischemic brain injury. It was identified that LINC00319 was significantly upregulated in the Gene Expression Omnibus profile of ischemic stroke. Furthermore, LINC00319 overexpression elevated caspase-3 activity and increased the apoptotic rate of neuronal cells, as well as decreased cell viability and glucose uptake. It was also demonstrated that LINC00319 participated in oxygen-glucose deprivation (OGD)-induced cerebral ischemic injury. LINC00319 could competitively bind with microRNA (miR)-200a-3p and decrease its expression. Moreover, miR-200a-3p could partly offset the negative effects of LINC00319 overexpression on neuronal injury caused by OGD. Collectively, the present results suggested that LINC00319 promoted apoptosis and aggravated neuronal injury induced by OGD by regulating miR-200a-3p, which may be important for ischemic stroke treatment.