中华眼外伤职业眼病杂志
中華眼外傷職業眼病雜誌
중화안외상직업안병잡지
Chinese Journal of ocular trauma and occupational eye disease
2015年
8期
580-584
,共5页
杨丽华%郝尚臣%徐玉灿%李志松%张卫
楊麗華%郝尚臣%徐玉燦%李誌鬆%張衛
양려화%학상신%서옥찬%리지송%장위
认知障碍%右美托咪定%天冬氨酸特异性半胱氨酰蛋白酶%细胞凋亡%晶状体囊外摘出术
認知障礙%右美託咪定%天鼕氨痠特異性半胱氨酰蛋白酶%細胞凋亡%晶狀體囊外摘齣術
인지장애%우미탁미정%천동안산특이성반광안선단백매%세포조망%정상체낭외적출술
Disorders,cognition%Dexmedetomidine%Cycteinyl aspirate-specific protease%Apoptosis%Extracapsular lens extraction
目的 探讨右美托咪定(Dexmedetomidine,Dex)对晶状体囊外摘出术(ECLE)后小鼠远期认知功能的作用.方法 实验用成年雄性C57BL/6J小鼠40只,采用随机数字表法分为对照组(C组)、ECLE组、生理盐水组(NS组)和Dex组,每组10只.ECLE模型制备后3d,C组和ECLE组进行Morris水迷宫试验,检测海马组织湿/干重比(W/D)和总含水量(TWC),逆转录-聚合酶链反应和蛋白免疫印迹法分别检测海马组织天冬氨酸特异性半胱氨酰蛋白酶(caspase)-12 mRNA及蛋白表达水平,原位末端细胞凋亡法检测海马组织细胞凋亡指数(AI).Dex组小鼠术毕苏醒即刻经腹腔注射Dex 25 μg·kg-1·d-1,NS组给予等容量生理盐水,连续30 d,随后检测前述项目.结果 与C组比较,ECLE组小鼠逃避潜伏期及游泳距离均延长(P<0.05),海马组织W/D、TWC及AI均增加(P<0.05),海马组织caspase-12 mRNA及蛋白表达水平均增加(P<0.05).与NS组比较,Dex组小鼠逃避潜伏期及游泳距离均缩短(P<0.05),海马组织W/D、TWC及AI均减少(P<0.05),海马组织caspase-12 mRNA及蛋白表达水平均降低(P<0.05).结论 Dex可改善ECLE后小鼠远期认知功能,其机制可能与其抑制海马组织caspase-12介导的细胞凋亡有关.
目的 探討右美託咪定(Dexmedetomidine,Dex)對晶狀體囊外摘齣術(ECLE)後小鼠遠期認知功能的作用.方法 實驗用成年雄性C57BL/6J小鼠40隻,採用隨機數字錶法分為對照組(C組)、ECLE組、生理鹽水組(NS組)和Dex組,每組10隻.ECLE模型製備後3d,C組和ECLE組進行Morris水迷宮試驗,檢測海馬組織濕/榦重比(W/D)和總含水量(TWC),逆轉錄-聚閤酶鏈反應和蛋白免疫印跡法分彆檢測海馬組織天鼕氨痠特異性半胱氨酰蛋白酶(caspase)-12 mRNA及蛋白錶達水平,原位末耑細胞凋亡法檢測海馬組織細胞凋亡指數(AI).Dex組小鼠術畢囌醒即刻經腹腔註射Dex 25 μg·kg-1·d-1,NS組給予等容量生理鹽水,連續30 d,隨後檢測前述項目.結果 與C組比較,ECLE組小鼠逃避潛伏期及遊泳距離均延長(P<0.05),海馬組織W/D、TWC及AI均增加(P<0.05),海馬組織caspase-12 mRNA及蛋白錶達水平均增加(P<0.05).與NS組比較,Dex組小鼠逃避潛伏期及遊泳距離均縮短(P<0.05),海馬組織W/D、TWC及AI均減少(P<0.05),海馬組織caspase-12 mRNA及蛋白錶達水平均降低(P<0.05).結論 Dex可改善ECLE後小鼠遠期認知功能,其機製可能與其抑製海馬組織caspase-12介導的細胞凋亡有關.
목적 탐토우미탁미정(Dexmedetomidine,Dex)대정상체낭외적출술(ECLE)후소서원기인지공능적작용.방법 실험용성년웅성C57BL/6J소서40지,채용수궤수자표법분위대조조(C조)、ECLE조、생리염수조(NS조)화Dex조,매조10지.ECLE모형제비후3d,C조화ECLE조진행Morris수미궁시험,검측해마조직습/간중비(W/D)화총함수량(TWC),역전록-취합매련반응화단백면역인적법분별검측해마조직천동안산특이성반광안선단백매(caspase)-12 mRNA급단백표체수평,원위말단세포조망법검측해마조직세포조망지수(AI).Dex조소서술필소성즉각경복강주사Dex 25 μg·kg-1·d-1,NS조급여등용량생리염수,련속30 d,수후검측전술항목.결과 여C조비교,ECLE조소서도피잠복기급유영거리균연장(P<0.05),해마조직W/D、TWC급AI균증가(P<0.05),해마조직caspase-12 mRNA급단백표체수평균증가(P<0.05).여NS조비교,Dex조소서도피잠복기급유영거리균축단(P<0.05),해마조직W/D、TWC급AI균감소(P<0.05),해마조직caspase-12 mRNA급단백표체수평균강저(P<0.05).결론 Dex가개선ECLE후소서원기인지공능,기궤제가능여기억제해마조직caspase-12개도적세포조망유관.
Objective To investigate the effect of Dexmedetomidine (Dex) on long-term cognitive function after extracapsular lens extraction (ECLE) in mice.Methods Forty adult male C57BL/6J mice were randomly divided into control group (C group),ECLE group,normal saline group (NS group) and Dex group with 10 mice in each group.Three days after ECLE model was made,the mouse in C group and ECLE group underwent Morris water maze test,then they were euthanized and hippocampus tissue was immediately excised for determination of wet weight to dry weight (W/D) and total water content (TWC).The transcription levels of cycteinyl aspirate-specific protease-12 (caspase-12) mRNA and its protein in hippocampus tissue were detected respectively by reverse transcription polymerase chain reaction (PCR) and Western Blot.Apoptosis index (AI) of hippocampus tissue was determined by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling assay.After the mice regained consciousness post the operation,animals received intraperitoneally Dex at a dose of 25 μg · kg-1 · d-1 for 30 consecutive days in Dex group.Animals of NS group were accepted intraperitoneally injection with the same volume of normal saline.The evaluation indexes mentioned above were programmed at 30 dyas post intraperitonedlly injection.Results Compared with C group,the escape latency and swimming distance were prolonged transcription in ECLE group (both P < 0.05),the value of W/D,TWC and AI were increased (all P < 0.05),and the expression of caspase-12 and mRNA transcription in hippocampus tissue were significantly higher (both P < 0.05) in ECLE group.Compared with NS group,the escape latency and swimming distance were shortened in Dex group(both P < 0.05),the value of W/D,TWC and AI were decreased (all P < 0.05),and the expression of caspase-12 and mRNA protein transcription in hippocampus tissue were significantly lower (both P < 0.05) in Dex group.Conclusion The treatment of Dex could improve the long-term cognitive function after ECLE in mice,and the mechanism may be through inhibiting apoptosis mediated by caspase-12 in hippocampus tissue.