中国行为医学科学
中國行為醫學科學
중국행위의학과학
2008年
11期
968-971
,共4页
张永平%于立坚%马润娣%张霄瑜%于廷曦
張永平%于立堅%馬潤娣%張霄瑜%于廷晞
장영평%우립견%마윤제%장소유%우정희
兴奋性毒性%阿魏酸钠%脑修复%幼小鼠
興奮性毒性%阿魏痠鈉%腦脩複%幼小鼠
흥강성독성%아위산납%뇌수복%유소서
Excitotoxicity%Sodium ferulate%Brain repair%Infant mice
目的 研究阿魏酸钠(SF)腹腔注射对妊娠晚期母小鼠谷氨酸单钠(MSG)灌胃诱导的仔鼠兴奋性毒性神经损伤修复的影响.方法 将妊娠17d小鼠随机分为:对照、SF、MSG、MSG+SF组.每组10只.MSG组小鼠在妊娠第17天接受MSG(1.0,2.0,4.0g/kg)灌胃1次.MSG+SF组和SF组小鼠在妊娠第17天分别接受MSG(4.0g/kg)或生理盐水灌胃1次,从妊娠第18天起腹腔注射SF(40mg/kg),每日1次,连续2~3d;子代小鼠出生后继续腹腔注射SF(40mg/kg),每日1次,连续20d.仔鼠31 d龄进行爬绳和开野实验,32d龄开始Y迷宫实验;在新生鼠24h、21 d龄和53 d龄,每组各取4只小鼠行脑海马组织病理学检查.结果 MSG组子代小鼠的自主活动次数增加非常显著(P<0.01);会爬绳者(5/13)较对照组(12/14)非常显著地减少(P<0.01);52d龄仔鼠Y迷宫正确反应次数(17.1/20)明显少于对照组(19.4/20)(P<0.01).MSG组小鼠海马神经细胞水肿、变性坏死和组织增生.然而,MSG+SF组31日龄子代小鼠自主活动次数明显少于MSG组(P<0.01);MSG+SF组会爬绳仔鼠(10/13)较MSG组(5/13)明显增多(P<0.05);52d龄MSG+SF组仔鼠Y迷宫正确反应次数(19.1/20)明显多于MSG组(17.1/20)(P<0.05);MSG+SF组仔鼠海马神经元的损伤部分或大部分修复.结论 母鼠和仔鼠长期腹腔注射SF对母鼠妊娠晚期MSG诱导的仔鼠的兴奋性毒性神经损伤有一定的修复作用.
目的 研究阿魏痠鈉(SF)腹腔註射對妊娠晚期母小鼠穀氨痠單鈉(MSG)灌胃誘導的仔鼠興奮性毒性神經損傷脩複的影響.方法 將妊娠17d小鼠隨機分為:對照、SF、MSG、MSG+SF組.每組10隻.MSG組小鼠在妊娠第17天接受MSG(1.0,2.0,4.0g/kg)灌胃1次.MSG+SF組和SF組小鼠在妊娠第17天分彆接受MSG(4.0g/kg)或生理鹽水灌胃1次,從妊娠第18天起腹腔註射SF(40mg/kg),每日1次,連續2~3d;子代小鼠齣生後繼續腹腔註射SF(40mg/kg),每日1次,連續20d.仔鼠31 d齡進行爬繩和開野實驗,32d齡開始Y迷宮實驗;在新生鼠24h、21 d齡和53 d齡,每組各取4隻小鼠行腦海馬組織病理學檢查.結果 MSG組子代小鼠的自主活動次數增加非常顯著(P<0.01);會爬繩者(5/13)較對照組(12/14)非常顯著地減少(P<0.01);52d齡仔鼠Y迷宮正確反應次數(17.1/20)明顯少于對照組(19.4/20)(P<0.01).MSG組小鼠海馬神經細胞水腫、變性壞死和組織增生.然而,MSG+SF組31日齡子代小鼠自主活動次數明顯少于MSG組(P<0.01);MSG+SF組會爬繩仔鼠(10/13)較MSG組(5/13)明顯增多(P<0.05);52d齡MSG+SF組仔鼠Y迷宮正確反應次數(19.1/20)明顯多于MSG組(17.1/20)(P<0.05);MSG+SF組仔鼠海馬神經元的損傷部分或大部分脩複.結論 母鼠和仔鼠長期腹腔註射SF對母鼠妊娠晚期MSG誘導的仔鼠的興奮性毒性神經損傷有一定的脩複作用.
목적 연구아위산납(SF)복강주사대임신만기모소서곡안산단납(MSG)관위유도적자서흥강성독성신경손상수복적영향.방법 장임신17d소서수궤분위:대조、SF、MSG、MSG+SF조.매조10지.MSG조소서재임신제17천접수MSG(1.0,2.0,4.0g/kg)관위1차.MSG+SF조화SF조소서재임신제17천분별접수MSG(4.0g/kg)혹생리염수관위1차,종임신제18천기복강주사SF(40mg/kg),매일1차,련속2~3d;자대소서출생후계속복강주사SF(40mg/kg),매일1차,련속20d.자서31 d령진행파승화개야실험,32d령개시Y미궁실험;재신생서24h、21 d령화53 d령,매조각취4지소서행뇌해마조직병이학검사.결과 MSG조자대소서적자주활동차수증가비상현저(P<0.01);회파승자(5/13)교대조조(12/14)비상현저지감소(P<0.01);52d령자서Y미궁정학반응차수(17.1/20)명현소우대조조(19.4/20)(P<0.01).MSG조소서해마신경세포수종、변성배사화조직증생.연이,MSG+SF조31일령자대소서자주활동차수명현소우MSG조(P<0.01);MSG+SF조회파승자서(10/13)교MSG조(5/13)명현증다(P<0.05);52d령MSG+SF조자서Y미궁정학반응차수(19.1/20)명현다우MSG조(17.1/20)(P<0.05);MSG+SF조자서해마신경원적손상부분혹대부분수복.결론 모서화자서장기복강주사SF대모서임신만기MSG유도적자서적흥강성독성신경손상유일정적수복작용.
Objective To investigate the effects of administered sodium ferulate (SF) on the repair of glutamate-induced excitotoxic neuronal impairment in mouse fetal brain.Methods Pregnant females were randomly divided into control,SF,MSG,and MSG + SF groups,n=10.The animals in MSG group received ig administration of monosodium glutamate (MSG,1.0,2.0,4.0g/kg,onee) at 17-day.The animals in MSG + SF and SF groups received ig administration of MSG (4.0g/kg,once) or normal saline at 17day,and ip administration of SF (40 mg/kg) starting at 18 dpo,once-daily for 2~3 d;the infant mice from the mothers treated with MSG +SF received ip administration of SF (40 mg/kg) after the birth,once-daily for 20 days.The animals in control and MSG groups received ig or ip administration of normal saline simultaneously,respectively.At the 31 st day after the birth the behavioural tests were performed,and the histopathology of the animal brains was studied.Results At the 31 st day after the birth,the number of MSG-treated mice which could crawl along a rope (5/13) was obviously less than that of control(12/14) (P<0.01) ;at the 52th day after the birth,correct responses of MSG-treated group in Ymaze test (17.1/20) were significantly less than that of control (19.4/20)(P<0.01).Examination of histopathology displayed MSG-induced hippocampal lesions were characterized by intracellular edema,degeneration and necrosis of neurons,and hyperplasia.However,the number of MSG+ SF-treated mice which could crawl along a rope (10/13) was close to that of control (12/14);at the 52th day after the birth,correct responses of Y-maze test in the MSG + SF group (19.1/20) were close those in the control (19.4/20).Examination of histopathology displayed that slight hippocampal lesions appeared in the MSG + SF-treated mice.Conclusion Long-term administration of SF may be feasible in repairing glutamate-induced exeitotoxic neuronal impairment in infant mice.