出 处:《中华神经医学杂志》2018年第5期457-461,共5页Chinese Journal of Neuromedicine
摘 要:目的 探讨神经节苷脂GM1对新生大鼠缺氧缺血性脑损伤(HIBD)的作用及对海马K+-Cl-协同转运蛋白2(KCC2)表达的影响. 方法 72只7d龄新生SD大鼠按随机数字表法分为假手术组、HIBD模型组和神经节苷脂GM1组,各组又依据检测指标的不同分为3d亚组和21d亚组,每亚组12只.后2组参考Rice-Vannucci法建立HIBD模型,神经节苷脂GM1组于造模后即刻予神经节苷脂GM1 20 mg/(kg·d)腹腔注射,连续给药3d.采用2,3,5-三苯基氯化四氮唑(TTC)法检测各3d亚组脑梗死体积比率,自主活动记录仪观察记录各21d亚组的自主活动情况,Morris水迷宫实验评估各21d亚组的学习记忆能力,Western blotting检测各3d、21d亚组海马组织KCC2蛋白的表达. 结果 与HIBD模型组[(28.6±5.2)%]相比,神经节苷脂GM1组脑梗死体积比[(11.3±2.4)%]明显降低,差异有统计学意义(P<0.05).与HIBD模型组[(289.6±61.3)次]比较,神经节苷脂GM1组2h内自主活动数[(412.1±66.8)次]明显增加,差异有统计学意义(P<0.05).与HIBD模型组比较,神经节苷脂GM1组逃逸潜伏期明显降低,穿越原平台次数和目标象限停留时间百分比均明显升高,差异均有统计学意义(P<0.05).神经节苷脂GM1组3d、21d亚组海马组织KCC2蛋白的表达较相应时间点的HIBD模型组均明显增高,差异均有统计学意义(P<0.05). 结论 神经节苷脂GM1对新生大鼠HIBD具有显著保护作用,机制可能与其调节海马KCC2的表达有关.Objective To evaluate the effects of ganglioside GM1 on hypoxic ischemic brain damage (HIBD) in neonatal rats and on the expression of potassium-chloride cotransporter 2 (KCC2) in hippocampus.Methods Seven-day-old Sprague-Dawley (SD) rats (n=72) were randomly divided into a sham group,an HIBD group and a ganglioside GM1 group.Each group was further divided into a 3 d subgroup and a 21 d subgroup according to the different detection index (n=12).Rat HIBD models were prepared according the Rice-Vannucci method.After HIBD,the ganglioside GM1 group was given ganglioside GM1 20 mg/ (kg ·d) by intraperitoneal injection for 3 d continuously.2-,3-,5-triphenyltetrazolium chloride (TTC) was preformed to evaluate the area of cerebral infarction of HIBD in each 3 d subgroup.Spontaneous activity recorder was used to observe the locomotor activity of the rats in the 21 d subgroups.Morris water maze test was conducted for assessment of rats' learning and memory abilities in the 21 d subgroups.Western blot analysis was employed to determine the alterations in KCC2 expression in hippocampus in all the 3 d and 21 d subgroups.Results Compared with the HIBD group (28.6%±5.2%),the ratio of cerebral infarction volume in the ganglioside GM1 group (11.3%±2.4%) was significantly reduced (P<0.05).Compared with the HIBD group (289.6±61.3),the number of locomotor activities within 2 h in the ganglioside GM1 group (412.1±66.8) was significantly increased (P<0.05).Compared with the HIBD group,the escape latency was significantly reduced,but the percentage time of target quadrant and the number of crossing the platform were significantly increased in the ganglioside GM1 group (P<0.05).Three days and 21 days after HIBD,the expression of KCC2 in the ganglioside GM1 group was significantly higher than that in the HIBD group (P<0.05).Conclusion Ganglioside GM1 may have a significant protective effect on HIBD in neonatal rats,and its mechanism may be related to regul
关 键 词:神经节苷脂GM1 缺氧缺血性脑损伤 K^+-Cl^-协同转运蛋白2
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