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为研究神经节苷脂GM1对新生大鼠缺氧缺血后神经细胞凋亡的影响,将63只7日龄SD大鼠分为4组:假手术组,对照组、保护组、治疗组,制成缺氧缺血性脑损伤(HIBD)模型,分别于缺氧缺血(HI)前及HI后腹腔注射GM1和生理盐水,通过HE染色、原位末端脱氧核糖核酸转移酶介导的生物素化的脱氧尿苷三磷酸缺口末端标记(TUNEL)和电镜观察,比较各组神经细胞凋亡。结果显示对照组阳性细胞数明显高于保护组、治疗组(t=7.16,5.08,p<0.01),且治疗组与保护组相比,阳性细胞数无明显差异(t=1.85,p>0.05)。本实验显示GM1确实能减少新生大鼠脑组织缺氧缺血后海马CA1区细胞凋亡,且GM1在HI前或后应用同样有效。
To investigate the effect of ganglioside GM1 on neuronal apoptosis in neonatal rats after hypoxia-ischemia, 63 7-day-old SD rats were divided into 4 groups: sham operation group, control group, protection group, treatment group, (HIBD) models were established. Hypoxic-ischemic brain damage (HIBD) models were established. Both GM1 and normal saline were injected intraperitoneally before and after hypoxia-ischemia (HI). HE staining, in-situ terminal deoxynucleotidyl transferase mediated TUNEL and electron microscopy were used to observe the apoptosis of nerve cells in each group. The results showed that the number of positive cells in the control group was significantly higher than that in the protection group and the treatment group (t = 7.16,5.08, p <0.01). There was no significant difference in the number of positive cells between the treatment group and the protection group (t = 1.85, p> 0.05 ). This experiment shows that GM1 can indeed reduce neonatal rat brain tissue hypoxic-ischemic hippocampal CA1 apoptosis, and GM1 before or after HI is equally effective.