To investigate the impacts of ferulic acid (FA) on jumonji C domain-containing protein 6 (JMJD6) and synaptophysin in the tissues of the hippocampus in neonatal and juvenile rats with intrauterine hypoxia-induced cognitive impairment. The Sprague-Dawley pregnant rats were randomly divided into three groups: control, hypoxia, and hypoxia + FA. On day 14 of pregnancy, the intrauterine hypoxia model was created by placing pregnant rats in the hypoxic and low-pressure experimental chamber for 2 hr a day for 3 days. In the hypoxia + FA group, pregnant rats were injected intraperitoneally with 4% FA, once a day for 7 days. The hypoxia group was treated with equal amounts of saline. After delivery, JMJD6 and synaptophysin mRNA and proteins in the hippocampus regions were detected by in situ hybridization and western blotting. The Morris water maze was used to evaluate cognitive function. The neonatal and juvenile rats in the hypoxia group had significantly increased expression of JMJD6 and decreased expression of synaptophysin protein and synaptophysin I mRNA in the hippocampus than those in the control group. Meanwhile, hypoxia also clearly prolonged the escape latency and shortened the stay time in the target quadrant. FA decreased the expression of JMJD6 and increased the expression of synaptophysin and improved cognitive function compared with those in the hypoxia group. FA probably ameliorated the cognitive impairment by regulating JMJD6 and synaptophysin in the hippocampus of neonatal and juvenile rats who had intrauterine hypoxia during pregnancy.
Keywords: JMJD6; cognitive impairment; ferulic acid; hippocampus; intrauterine hypoxia; synaptophysin.
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