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目的观察托吡酯对新生大鼠脑白质损伤的保护作用。方法采用右侧颈总动脉结扎加缺氧处理的2日龄SD大鼠脑白质损伤(White Matter Damage,WMD)模型,检测WMD模型后12 h、24 h、48 h及72 h脑白质丙二醛(Malondialdehyde,MDA)和超氧化物歧化酶(Superoxide Dismutase,SOD)含量的改变,并与对照组大鼠比较。WMD模型组大鼠分别加用托吡酯30 mg/kg(托吡酯干预组)和DMSO(非干预组)腹腔注射5次后检测脑白质MDA的改变,电镜观察大鼠脑白质髓鞘化形成情况。结果 WMD各组大鼠脑白质MDA含量明显高于对照组(P<0.001),SOD活性低于对照组(P<0.001);托吡酯干预组MDA水平明显低于非干预组(P<0.001)。电镜观察显示,托吡酯干预组大鼠脑白质髓鞘化程度明显好于非干预组。结论新生大鼠脑缺氧缺血后,脑白质SOD含量下降,MDA随着缺氧缺血时间的延长而生成增多;托吡酯对新生大鼠脑白质损伤具有保护作用。
Objective To observe the protective effect of topiramate on white matter damage in neonatal rats. Methods The white Matter Damage (WMD) model of 2-day-old Sprague-Dawley rats was used to detect the effects of carotid artery occlusion and hypoxia on the right ventricle at 12 h, 24 h, 48 h and 72 h after WMD. Malondialdehyde (MDA) and superoxide dismutase (SOD) were measured and compared with the control group. Rats in WMD model group were treated with topiramate 30 mg / kg (topiramate intervention group) and DMSO (non-intervention group) intraperitoneally 5 times respectively. The changes of MDA in the white matter of the WMD model group were observed. Results The content of MDA in white matter of rats in WMD group was significantly higher than that in control group (P <0.001), and the activity of SOD was lower than that in control group (P <0.001). The level of MDA in topiramate intervention group was significantly lower than that in non-intervention group (P <0.001). Electron microscopy showed that topiramate in the topiramate intervention group was significantly better than the non-intervention group. Conclusions After hypoxic-ischemic brain damage in neonatal rats, the content of SOD in brain white matter decreases and MDA increases with the prolongation of hypoxic-ischemic time. Topiramate has a protective effect on white matter damage in neonatal rats.