摘要
建立新生鼠缺氧缺血性脑病（HIE）的模型，观察了大脑皮质超氧化物歧化酶（SOD）、丙二醛（MDA）、血清MDA和脑组织神经病理变化以及硫酸镁、川芎嗪对其影响。发现HIE组大脑皮质SOD、MDA和血清MDA升高明显，神经细胞变性显著。硫酸镁和川芎嗪能使大脑皮质SOD、MDA和血清MDA降低，神经细胞变性减轻。提示氧自由基在缺氧缺血性脑损害发病中的影响和硫酸镁、川芎嗪通过间接抗氧化作用对HIE的预防作用。
Objective A model in neonatal rats was established to study pathophysiology of perinatal hypoxic-ischemic brain damage. Methods 7-9 day old Wistar rats were subjected to unilateral carotied artery ligation followed by hypoxic state for 3 hours (10% O2 + 90%N2, at 37℃). Magnesium sulfate (0. 5 mg/gBW) and ligustrazin (0. 1 mg/gBW) was separately given a 30 min before hypoxia. Superoxide dismutase(SOD) and malonic dialdehyde (MDA) in the cerebral cortex and serum MDA were measured immediately after hypoxia. Neuropathologic examination was made in 4 weeks after hypoxia. Results It was found that SOD and MDA in the cerebral cortex and serum MDA in the hypoxicischemic group were significantly increased in cornparision with the normal control group(P<0. 01 ). and that all these parameters either in the magnesium sulfate group or in the ligustrazin group were lower than in the hypoxic-ischemic group (P<0. 05). Th e hypoxic-ischemic group showed that there were neuronal degenerations in the gray matter, hippocampus and cerebellum which were reduced in the two treatment groups. Conclusion Our results indicate that oxide free radical formation is one of the pathogenic factors of perinatal hypoxic-ischemic brain damage and magnesium sulfate and ligustrazin reduce hypoxicischemic brain damage due to indirect anti-oxidation.
出处
《中国医学科学院学报》
CAS
CSCD
北大核心
1997年第4期301-304,共4页
Acta Academiae Medicinae Sinicae
基金
中国医学科学院科学基金
关键词
缺氧缺血性脑病
硫酸镁
川芎嗪
预防
新生儿
hypoxic-ischemic encephalopathy
neonatal rat
magnesium sulfate
ligustrazin
