神经节苷脂GM1对新生大鼠缺氧缺血后海马CA1区神经细胞凋亡的影响

INFLUENCE OF GANGLIOSIDE GMl ON NEURONAL APOPTOSK OF CAl PY- RAMIDAL CELL LAYER OF HIPPOCAMPUS AFTER HYPOXIA-ISCHEMIA IN THE NEONATAL RATS

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。

In order to study the influence of ganglioside GM1 on neuronal apotosis after hypoxia-ischemia( HI) in the neonatal rats, 63 7-day-old Sprague-Dawley rats were studied, divided into 4 groups: sham-operated grouop, control group, protection group and treatment group. After hypoxic-ischemic brain damage (HIBD) models having been produced, GM1 and saline were injected from peritone before or after HI. Compare each group's neuronal apoptosis with Hematoxyline and Eosine(Hand E) staining, terminal de-oxynucleotidyl dUTP-biotin in situ nick end labeling (TUNEL) and electron - microscopy. Results showed that the neuronal apoptosis of control group was much more than that of protection group and treatment group (t = 7.16,5.08 respectively, P < 0.01) . Moreover, there was no remarkable difference between protection group and treatment group (t= 1.85, P > 0.05 ) . Therefore, it suggests that GM1 do reduce apoptosis of CA1 pyramidal cell layer of hippocampus after hypoxia-ischemia. GM1 has the same efficacy on reducing apoptosis after HI as before HI.