Effects of dexmedetomidine on neurological function in neonatal rats with hypoxicischemic encephalopathy
BO Lijun1， YU Peixia2, HUANG Lining1， Xue Hui3， Kang RongTian1*
2017, 37(9):
1068-1071,1075.
doi:10.3969/j.issn.10073205.2017.09.018
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［Abstract］ Objective〖HTSS〗〓To observe the effect of dexmedetomidine on neuronal apoptosis in neonatal rats with cerebral ischemia and hypoxia, and to explore the effect of dexmedemidine on neurological function and longterm learning and memory ability.
〖HTH〗〖WTHZ〗Methods〖HTSS〗〓Hypoxicischemic encephalopathy(HIE) was built for the model of cerebral ischemia and hypoxia. Ninety sevendayold(P7) SpragueDawley rats were randomized into five groups: sham operation group(S), the HIE group(R), the dexmedetomidine(25 μg/kg) group(D1), the dexmedetomidine(50 μg/kg) group(D2), the yohimbine group(5 μg)(Y). P7 rats were operated without hypoxia in S group, and continued hypoxia for 2 h in R group. After HIE 2 h, P7 rats were pretreated with different concentrations of dexmedetomidine(25 μg/kg,) in D1 group, and pretreated with dexmedetomidine(50 μg/kg) in D2 group and yohimbine(5 μg) in Y group. After 24 h, the expression of caspase3 was detected. Neurological deficit scores were used to evaluate neurological function. For 4 weeks after the intervention, Morris water maze test was used to evaluate the changes in learning and memory ability.
〖HTH〗〖WTHZ〗Results〖HTSS〗〓HIE in R group induced the upregulation of caspase3 and neurological deficit scores, compared with S group（P＜005）. Dexmedetomidine(25 μg/kg, 50 μg/kg) and yohimbine pretreatment markedly downregulated the expression of caspase3 and neurological deficit scores, compared with R group（P＜005）. The escape latency of R group was increased compared with S group, and reduced with D1, D2, Y group at 2th,3th,4th and 5th day after training（P＜005）. The escape latency of both D1 and D2 group were reduced at 2th,3th,4th and 5th day, and increased time of target quadrant compared with R group, and reduced compared with S group（P＜005）. Neurological deficit scores and the expression of caspase3 were significantly reduced in Y group compared with D1 and D2 group（P＜005）. There were not significant differences between D1 and D2 group in neurological deficit scores, the expression of caspase3 and Morris water maze test.
〖HTH〗〖WTHZ〗Conclusion〖HTSS〗〓 HIE causes neuronal apoptosis in the hippocampus of neonatal rats, and decrease the ability of learning ang memory in longterm neonatal rats. The expression of caspase3 was inhibited by dexmedetomidine pretreatment(25 μg/kg, 50 μg/kg), which reduced the apoptosis of neurons . Dexmedetomidine treatment for neonatal rats during HIE could improve the longterm learning and memory ability of neonatal rats.
