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目的探讨缺血后处理(IPostc)对新生大鼠缺氧缺血性脑损伤(HIBD)可能的神经保护作用及其机制。方法以7日龄SD大鼠为研究对象,随机分为假手术组、HIBD组、IPostcⅠ组(15 s再灌注/15 s夹闭×3个循环)及IPostcⅡ组(30 s再灌注/10 s夹闭×3个循环),每组根据缺氧缺血后时间分为0、6、12、24 h及48 h 5个亚组,每个亚组15只。应用右侧颈总动脉夹闭联合低氧(8%O2+92%N2)建立HIBD模型,监测脑组织形态学变化,比较超氧化物歧化酶(SOD)、丙二醛(MDA)、脑组织含水量及水通道蛋白4(AQP4)mRNA相对表达量随时间的变化规律。结果经缺氧缺血处理的大鼠均出现典型的神经行为学异常、形态学和生化指标的变化。IPostcⅠ组SOD活性显著改善,MDA含量降低,脑组织含水量及AQP4 mRNA相对表达量降低,在6 h以后作用显著,差异有统计学意义(P<0.05)。而IPostcⅡ组无明显改善作用。结论缺血后处理对新生大鼠HIBD具有一定的神经保护作用,其机制与减轻氧化应激损伤及脑水肿有关。
Objective To investigate the possible neuroprotective effect of IPostc on hypoxic-ischemic brain damage (HIBD) in neonatal rats and its mechanism. Methods Seven-day-old SD rats were randomly divided into three groups: sham operation group, HIBD group, IPostcⅠ group (15 s reperfusion / 15 s clipping × 3 cycles) and IPostcⅡ group (30 s reperfusion / 10 s Closure × 3 cycles), each group according to the time after hypoxia and ischemia were divided into 0, 6, 12, 24 h and 48 h 5 subgroups, 15 in each subgroup. HIBD model was established by occlusion of right common carotid artery and hypoxia (8% O2 + 92% N2). The morphological changes of brain were observed. The activities of superoxide dismutase (SOD), malondialdehyde (MDA) Water content and the expression of AQP4 mRNA with time. Results Hypoxic-ischemic rats showed typical neurobehavioral abnormalities, morphological and biochemical changes. The activity of SOD in IPostc I group was significantly improved, the content of MDA was decreased, the content of water in brain tissue and the relative expression of AQP4 mRNA in brain tissue were decreased, and the effect was significant after 6 h (P <0.05). The IPostc Ⅱ group no significant improvement. Conclusion The ischemic postconditioning may have a neuroprotective effect on HIBD in neonatal rats. Its mechanism is related to the reduction of oxidative stress and cerebral edema.