Downregulation of miR-19a-3p by Ischemic Postconditioning Protects Hippocampal Neurons in Rats Following Cerebral IR Injury

Objective To explore the protective effect of downregulation of miR-19a-3p induced by ischemic postconditioning on hippocampal CA1 neurons in rats after global cerebral IR injury.Methods Eight patients freshly diagnosed with acute ischemic stroke（within 24 h） in the Department of Neurology of the Affiliated Hospital of Xuzhou Medical University and 8 healthy individuals in the same age range were enrolled in this study.The expression of miR-19a-3p in peripheral blood was detected.Then 109 SD rats were randomly divided into 7 groups, that is, sham operation（n=15）,cerebral IR（n=23）,ischemic postconditioning（n=23）,ischemic postconditioning+miR-19a-3p agonist（agonist, n=9）,ischemic postconditioning+agonist negative control（agonist NC,n=9）,cerebral IR+miR-19a-3p inhibitor（inhibitor, n=15）,and cerebral IR+inhibitor negative control（inhibitor NC,n=15） groups.qRT-PCR was used to detect the expression of miR-19a-3p.Their cognitive ability was observed with NOR task.Results The expression of miR-19a-3p in peripheral blood was significantly higher in the patients with acute ischemic stroke than the healthy individuals（P＜0.05）.The expression of miR-19a-3p was obviously higher in cerebral IR group than the sham operation group（P＜0.05）,while that in the ischemic postconditioning group was notably lower than that in the sham operation group and cerebral IR group（P＜0.05）.The ischemic postconditioning group had higher neuronal density in hippocampal CA1 region（170.20±8.01 vs 15.40±6.80,P＜0.01） and cognitive index [（65.12±7.68）% vs（50.30±5.95）%,P＜0.05].The neuronal density in hippocampal CA1 region was lower in the agonist group than the agonist NC group（P＜0.01）,while the density and cognitive index were obviously higher in the inhibitor group than the inhibitor NC group（P＜0.05,P＜0.01）.Conclusion Ischemic postconditioning inhibits the expression of miR-19a-3p in hippocampal CA1 region of rats after global cerebral IR injury, and downregulation of its expression level promotes the survival of hippocampal CA1 neurons and improves the cognitive function after the injury.