RESUMO
Previous human and animal studies demonstrated that voluntary exercise may improve cognitive function and facilitate neuronal plasticity in ischemia/reperfusion (I/R) models. However, the possible underlying mechanisms remain to be elucidated. Metastasisassociated lung adenocarcinoma transcript 1 (MALAT1), a long noncoding RNA (lncRNA), may be associated with the functions and dysfunctions of endothelial cells. The present study investigated whether spontaneous runningwheel (RW) exerciseinduced MALAT1 expression changes may be associated with the cognitive improvement of mice following I/R injury. The expression of MALAT1 was evaluated using reverse transcriptionquantitative polymerase chain reaction. Artificial MALAT1 and MALAT1 lentiviral mall interfering (siRNA) were used to alter MALAT1 expression levels in vivo. The Morris Water Maze test was performed to evaluate spatial learning and memory retention in the mice. Changes in the apoptotic rates of hippocampal neurons and levels of apoptosisassociated proteins were also detected. The data revealed that MALAT1 increased in the hippocampus of mice in the RWtreated I/R group and that this was associated with neurological, learning and memory improvement, reduced infarction volumes, decreased apoptosis and alterations to expression levels of apoptosisassociated proteins. Following RW training in I/Rinjured mice, lentiviral MALAT1 siRNA conduction partially attenuated the protections induced by voluntary RW. However, exogenous MALAT1 treatment increased the protection. The current findings suggested that voluntary RW protected hippocampal neurons from I/R injury and promoted cognitive restoration, which was associated with lncRNA MALAT1mediated apoptosis inhibition.