摘要
目的 研究外源性单唾液酸四己糖神经节苷脂(GM1)对新生鼠缺氧缺血脑损伤 (HIBD)的保护作用 .方法 结扎新生 7d龄 SD大鼠左颈总动脉后吸入 80 m L· L- 1 浓度氧 2 h,建立 HIBD模型 .观察腹腔注射 GM1对 HIBD模型鼠的体质量增长和脑水肿的影响 ,并用苏木素 -伊红 (HE)染色、原位缺口末端 (TUNEL )标记 DNA片段 ,检测凋亡细胞在大鼠海马和皮质的动态变化及 GM1对其的影响 .结果 外源性 GM1治疗促进了 HIBD模型鼠体质量增长 ,明显减轻了脑水肿及海马和皮质神经细胞凋亡 .结论 外源性 GM1对 HIBD后的脑组织确有保护作用 .
AIM To study the protective effects of monosialotetrahexosylganglioside (GM1) after hypoxic ischemic brain damage (HIBD) in neonatal rats. METHODS An animal model of neonatal hypoxic ischemic brain damage was set up by ligating the unilateral carotid artery of 7 day old SD rats and keeping the rats in a hypoxic (80 mL·L -1 oxygen) environment for 2 hours. Body weights and the degree of brain edema in HIBD rats treated with GM1 intraperitoneally were compared with that in HIBD rats without the treatment of GM1 (untreated group). The effect on apoptosis of neurons in the hippocampus and cortex was observed byhematoxylin eosin staining and terminal deoxynucleotidyl transferase mediated dUTP biotin nick end labeling (TUNEL) staining. RESULTS GM1 treatment relieved brain edema and brain injury, and decreased apoptosis of neurons in the hippocampus and cortex. CONCLUSION It is suggested that intraperitoneal administration with GM1 has cerebral protective effects on HIBD.
出处
《第四军医大学学报》
北大核心
2002年第17期1604-1607,共4页
Journal of the Fourth Military Medical University
关键词
脑缺血
脑缺氧
凋亡
GM1
cerebral ischemia
cerebral anoxia
apoptosis
GM1
