【摘要】 目的观察新生大鼠缺氧缺血(hypoxia-ischemia,HI)性脑损伤后脑细胞凋亡的情况,探讨单唾液酸四己糖神经节苷脂(single four hexose ganglioside sialic acid,GM1)对HI后神经元及凋亡相关基因Bax/Bcl-2表达的影响。方法选择新生7日龄SD新生大鼠108只,随机分为3组,缺氧缺血组(HI组),假手术对照组(control组),缺氧缺血+神经节苷脂组(GM1组)。每组36只。采用结扎右侧颈总动脉并吸入低氧混合气体制备缺氧缺血性脑损伤(hypoxia-ischemia brain damage,HIBD)模型。用原位末端转移酶标记技术法检测神经元凋亡情况,用免疫组织化学链霉亲合素生物素酶复合物法检测Bax/Bcl-2的表达。结果正常新生大鼠海马组织神经元凋亡率较低,与对照组比较HI组新生大鼠神经元凋亡明显增加(P<0.05),GM1可明显改善HI诱导的神经元凋亡。正常新生大鼠海马组织Bax和Bcl-2均有一定程度表达,HI可导致Bax表达增加,Bcl-2表达减少,腹腔给于GM1可逆转HI诱导的Bax和Bcl-2表达。结论 GM1可明显抑制HI诱导的神经元凋亡,调节Bax/Bcl-2表达可能是其脑保护的作用机制之一。更多还原

【Abstract】 Objective To study the brain cell apoptosis after hypoxic-ischemic brain damage (HIBD)in neonatal rats,and to discuss the effect of single four hexose ganglioside sialic acid (GM1)on neuronal apoptosis and the expression of apoptosis related gene Bax/Bcl-2. Methods One hundred and eight 7-day-old SD rats were divided at random into 3 groups,hypoxicischemic -group(HI group),sham operation control group(control group),hypoxic-ischemic-GM1 (GM1 group),with 36 rats in each group.Deligation of right common carotid artery and breathing in low-oxygen gas mixture were applied to prepare HIBD mode.TUNEL staining was applied in the detection of apoptosis.The expression of Bax/Bcl-2 was assayed by immunohistochemistry method.Results The neuronal apoptosis apoptosis rate in the hippocampus of nomal neonatal rats was relatively low Compared with control group,the neuronal apoptosis of rats in HI group increased significantly.GM1 could ameliorate neuronal apoptosis induced by HI obviously.Both Bax and Bcl-2 in the hippocampus of nomal neonatal rats showed positive expression.HI could enhance the expression of Bax and lessen the expression of Bcl-2.GM1 could reverse the effect of HI on the expression of Bax and Bcl-2.Conclusion GM1 can inhibit neuronal apoptosis induced by HI obviously.The regulation to the expression of Bax/Bcl-2 may be one of the cerebral protection mechanism of GM1.更多还原