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神经节苷脂对缺氧缺血新生鼠脑保护作用的研究
引用本文:殷宪敏,李睿,李静.神经节苷脂对缺氧缺血新生鼠脑保护作用的研究[J].泰山医学院学报,2006,27(6):513-515.
作者姓名:殷宪敏  李睿  李静
作者单位:泰山医学院附属医院,山东,泰安,271000
摘    要:目的探讨神经节苷脂GM-1对缺氧缺血新生鼠脑组织超氧化物岐化酶、丙二醛以及神经元凋亡的影响。方法7日龄Wistar大鼠70只,随机分成3组,①假手术组:仅做颈正中切口,不做颈总动脉结扎;(函治疗组(GM一1组),缺氧缺血性脑损伤(HIBD)后即刻腹腔内注射GM-110mg/kg;③对照组(生理盐水组),HIBD后即刻腹腔注射等体积的生理盐水。①于手术后即刻,②、③于处置后0、24、48、72h断头取脑,分别检测SOD/MDA的水平,并经HE和Tunel染色,光镜下检测海马CAI脑细胞凋亡数。结果观察组24、48、72h脑组织SOD的水平明显高于对照组,MDA的水平明显低于对照组,两组差异有显著性(P〈0.01),对照组大鼠海马CA1区可见典型的凋亡细胞,表现为细胞固缩、胞浆深染、核浓缩、碎片、核浆分布不清,有凋亡小体形成;GM-1组上述凋亡细胞明显减少;Tunel染色对照组阳性细胞数与GM-1组比较差异有明显的统计学意义(P〈0.05)。结论GM-1对HIBD有明显的保护作用。

关 键 词:脑缺氧  细胞凋亡
文章编号:1004-7115(2006)06-0513-03
收稿时间:2006-08-16
修稿时间:2006年8月16日

The study on protective effect of Gangliosides GMI on rat with hypoxic-ischemia
YIN Xian-min,LI Rui,LI jing.The study on protective effect of Gangliosides GMI on rat with hypoxic-ischemia[J].Journal of Taishan Medical College,2006,27(6):513-515.
Authors:YIN Xian-min  LI Rui  LI jing
Institution:Affiliated Hospital Taishan Medical College, Taian 271000,China
Abstract:Objective : To explore the influence of the Gangliosides GM-1 on the hypoxic-ischemic neonatal rat model.Methods:70 postnatal 7-day-old Wistar rats were randomly divided as follows:group 1(n=10),sham operation;group 2(n=30),GM-1 group,and gsoup 3(n=30),normal saline.GM-1(10 mg/kg)or normal saline was injected intraperitoneally into rats in group 2 or 3 after hypoxia(left carotid artery ligation)and ischemia.The rats were killed in 0,24,48 and 72 hours after hypoxic-ischemia to detect the level of SOD and NDA in rat brain and neuronal apoptosis in the hippocampal CAI regin was detected by HE and TUNEL staining.Results:In group 2,the level of SOD was higher than that in group 3;but the level of MDA was lower than that in group 3.In group 1,few apoptotic cells were detected.Average TUNEL-positive cells in group 2 were much more than more than those in group 3,there was significant difference between the two groups(P<0.01).Conclusion: GM-1 can protect the brain of rats with HIBD.
Keywords:GM-1  SOD  MDA
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