缺氧缺血新生大鼠海马ERK的变化及GM1的影响

目的:观察新生大鼠缺氧缺血性(HI)脑损伤后脑细胞凋亡的情况,进一步研究HI脑损伤后海马细胞外信号调节激酶(ERK)的变化,探讨单唾液酸四己糖神经节苷脂(GM1)对HI新生大鼠的脑保护作用。方法:选择新生7日龄Sprague-Dawley大鼠108只,随机分为3组:缺氧缺血组(HI组,36只),假手术对照组(Control组,36只),缺氧缺血+神经节苷脂组(GM1组,36只)。采用结扎右侧颈总动脉并吸入低氧混合气体制备HIBD模型,用TUNEL法检测细胞凋亡,免疫组化SP法检测大脑海马CA1区p-ERK的表达。结果:新生大鼠HI后脑细胞存在凋亡,GM1治疗能减少细胞凋亡。HI组、Control组和GM1组凋亡细胞数分别为(8.41±1.27)、(39.25±2.02)和(11.10±1.79),HI组阳性细胞数明显高于Control组和GMl组(P<0.05),GM1组与Control组比较阳性细胞数无明显差异(P>0.05)。HI组和GMl组p-ERK表达皆为阳性,两组比较HI组表达更强(P<0.05),Control组未见有p-ERK表达。结论:GM1可减少HI脑损伤后脑细胞凋亡,影响p-ERK表达,对缺氧缺血(HI)新生大鼠的脑具有保护作用。

The change of ERK expression and the effect of GM1 on the hippocampus of hypoxic - ischemic brain damage in neonatal rats

Objective:To observe the apoptosis of the brain cells and the changes of extracellular signal regulated kinase(ERK) expression in the hippocampus of hypoxic-ischemic brain damage in neonatal rats,disscuss the protectional effect of GM1 on neonatal rats' brain.Methods:108 cases of 7-day-old Sprague-Dawley rats were divided into 3 groups randomly:hypoxic-ischemic-group(HI group,36 cases),false-opration control group(control group,36 cases),hypoxic-ischemic rats injected by GM1 group(GM1 group,36 cases).Deligation of cephalic artery and breathing in low-oxygen gas mixture were applied to prepare HIBD models.TUNEL staining was applied to the detection of apoptosis.The expression of p-Erk in CA1 region of the hippocampus was assayed by immunohistochemistry SP method.Results:Brain cells apoptosis occured after hypoxic-ischemic brain damage in neonatal rats,GM1 inhibited the process.The number of apoptotic cells of HI group,control group and GM1 group were(8.41±1.27),(39.25±2.02) and(11.10±1.79),respectively.The number of positive cells in HI group was significangtly higher than that in control group and GMl group(P<0.05),and there was no significant difference between control group and GM1 group(P>0.05).The expression of p-ERK in HI group was higher than that in GM1 group(P<0.05).There was no positive expression of p-ERK in control group.Conclusion:GM1 can inhibit the cell apoptosis after hypoxic-ischemic brain damage and has certain effect on the expression of p-ERK,which can protect the brain of hypoxic-ischemic neonatal rats.