Inhibition of miRNA-210 reverses nicotine-induced brain hypoxic-ischemic injury in neonatal rats.

摘要: Maternal tobacco use in pregnancy increases the risk of neurodevelopmental disorders and neurobehavioral deficits postnatal life. The present study tested hypothesis that perinatal nicotine exposure exacerbated brain vulnerability to hypoxic-ischemic (HI) injury neonatal rats through up-regulation miR-210 expression developing brain. Nicotine was administered pregnant via subcutaneous osmotic minipumps. Experiments HI were performed 10-day-old pups. Perinatal treatment significantly decreased body weights, but increased weight ratio. caused a significant increase infarct size neonates. In addition, enhanced attenuated brain-derived neurotrophic factor (BDNF) tropomyosin-related kinase isoform B (TrkB) protein abundance Of importance, intracerebroventricular administration inhibitor (miR-210-LNA) HI-induced reversed nicotine-increased neonate. Furthermore, miR-210-LNA also nicotine-mediated down-regulation BDNF TrkB brains. These findings provide novel evidence plays causal role nicotine-induced developmental programming ischemic sensitive phenotype It represents potential therapeutic approach for encephalopathy neonate-induced by fetal stress.