中国临床康复
中國臨床康複
중국림상강복
CHINESE JOURNAL OF CLINICAL REHABILITATION
2005年
9期
230-231
,共2页
脑缺血%再灌注损伤%神经元%细胞凋亡%二异丙酚%基因
腦缺血%再灌註損傷%神經元%細胞凋亡%二異丙酚%基因
뇌결혈%재관주손상%신경원%세포조망%이이병분%기인
背景:异丙酚可能具有抗凋亡作用,从而保护脑缺血神经元耐受缺血性损伤.但是,异丙酚抗凋亡作用的机制还有待深入研究.目的:探讨异丙酚对全脑缺血再灌注损伤大鼠神经细胞凋亡和凋亡相关基因表达的影响.设计:随机对照的实验研究.单位:北京天坛医院神经外科.材料:实验于2003-01/2004-01在首都医科大学附属北京神经外科研究所进行研究.成年雄性Wistar大鼠23只,随机分为缺血组(9只)、异丙酚组(9只)和假手术对照组(5只).干预:制备大鼠全脑缺血再灌注模型.异丙酚组再灌注开始后立即静脉输注异丙酚1.5 mL/h,持续30 mino每组取5只大鼠于再灌注24 h取脑,用流式细胞仪检测凋亡率和坏死率.缺血组和异丙酚组各取4只大鼠,利用基因芯片结合图像分析技术检测凋亡相关基因的差异表达情况.主要观察指标:①凋亡率和坏死率.②基因芯片检测凋亡相关基因的差异表达情况.结果:异丙酚组海马神经元的凋亡率和坏死率[(7.01±0.79)%和(12.80±0.92)%]较缺血组[(10.89±0.80)%和(16.67±1.04)%]明显降低(P＜0.01).与缺血组比较,异丙酚组凋亡蛋白酶激活因子(apoptotic protease activatingfactor 1,PAF1)、DEFT和STM-2三个凋亡相关基因下调.结论:异丙酚具有脑保护作用,其机制可能与APAF1,EFT和STM-2三个凋亡相关基因下调有关.
揹景:異丙酚可能具有抗凋亡作用,從而保護腦缺血神經元耐受缺血性損傷.但是,異丙酚抗凋亡作用的機製還有待深入研究.目的:探討異丙酚對全腦缺血再灌註損傷大鼠神經細胞凋亡和凋亡相關基因錶達的影響.設計:隨機對照的實驗研究.單位:北京天罈醫院神經外科.材料:實驗于2003-01/2004-01在首都醫科大學附屬北京神經外科研究所進行研究.成年雄性Wistar大鼠23隻,隨機分為缺血組(9隻)、異丙酚組(9隻)和假手術對照組(5隻).榦預:製備大鼠全腦缺血再灌註模型.異丙酚組再灌註開始後立即靜脈輸註異丙酚1.5 mL/h,持續30 mino每組取5隻大鼠于再灌註24 h取腦,用流式細胞儀檢測凋亡率和壞死率.缺血組和異丙酚組各取4隻大鼠,利用基因芯片結閤圖像分析技術檢測凋亡相關基因的差異錶達情況.主要觀察指標:①凋亡率和壞死率.②基因芯片檢測凋亡相關基因的差異錶達情況.結果:異丙酚組海馬神經元的凋亡率和壞死率[(7.01±0.79)%和(12.80±0.92)%]較缺血組[(10.89±0.80)%和(16.67±1.04)%]明顯降低(P＜0.01).與缺血組比較,異丙酚組凋亡蛋白酶激活因子(apoptotic protease activatingfactor 1,PAF1)、DEFT和STM-2三箇凋亡相關基因下調.結論:異丙酚具有腦保護作用,其機製可能與APAF1,EFT和STM-2三箇凋亡相關基因下調有關.
배경:이병분가능구유항조망작용,종이보호뇌결혈신경원내수결혈성손상.단시,이병분항조망작용적궤제환유대심입연구.목적:탐토이병분대전뇌결혈재관주손상대서신경세포조망화조망상관기인표체적영향.설계:수궤대조적실험연구.단위:북경천단의원신경외과.재료:실험우2003-01/2004-01재수도의과대학부속북경신경외과연구소진행연구.성년웅성Wistar대서23지,수궤분위결혈조(9지)、이병분조(9지)화가수술대조조(5지).간예:제비대서전뇌결혈재관주모형.이병분조재관주개시후립즉정맥수주이병분1.5 mL/h,지속30 mino매조취5지대서우재관주24 h취뇌,용류식세포의검측조망솔화배사솔.결혈조화이병분조각취4지대서,이용기인심편결합도상분석기술검측조망상관기인적차이표체정황.주요관찰지표:①조망솔화배사솔.②기인심편검측조망상관기인적차이표체정황.결과:이병분조해마신경원적조망솔화배사솔[(7.01±0.79)%화(12.80±0.92)%]교결혈조[(10.89±0.80)%화(16.67±1.04)%]명현강저(P＜0.01).여결혈조비교,이병분조조망단백매격활인자(apoptotic protease activatingfactor 1,PAF1)、DEFT화STM-2삼개조망상관기인하조.결론:이병분구유뇌보호작용,기궤제가능여APAF1,EFT화STM-2삼개조망상관기인하조유관.
BACKGROUND: Disoprofol has anti-apoptosis impact so that it can protect the neurons from damage caused by ischemia. However, it needs further study on the mechanism of anti-apoptosis of it.
OBJECTIVE: To investigate the effects of disoprofol to cell apoptosis and expression of apoptosis-associated gene in rats during reperfusion after global ischemia.DESIGN: A randomized controlled trial.SETTING: Department of Neurosurgery of Beijing Tiantan Hospital.MATERIALS: The experiment was conducted in Beijing Neurological Surgery Research Institute of Capital University of Medical Sciences during January 2003 to January 2004. A total of 23 adult male Wistar rats were randomly divided into ischemic group( n =9), disoprofol group( n =9) and
sham operation group( n = 5).INTERVENTIONS: To prepare global ischemia-reperfusion model of rats. Disoprofol was injected into vein with dose of 1.5 mL/hour after reperfusion started in disoprofol group and lasted for 30 minutes. Five rats were selected from each group to be removed brain after reperfusion for 24 hours. Apoptosis rate and necrosis rate were detected by flow cytometer. Four rats selected from ischemic and disoprofol group were detected differential expression of apoptosis associated genes by gene chip combining image analysis techniques.MAIN OUTCOME MEASURES: ① apoptosis rate and necrosis rate; ②expression of apoptosis-associated gene detected by gene chip.RESULTS: The apoptosis rate[(7.01 ±0.79)% ] and necrosis rate[ ( 12. 80 ± 0. 92) % ] of neurons of hippocampus in disoprofol group were much lower than those of ischemic group [ (10. 89 ± 0. 80)%, (16. 67 ± 1.04)% ](P ＜ 0.01) . Compared with ischemic group, the three apoptosis associated genes including apoptotic prote ase activating factor 1 (APAF1), death effector domain containing testicular molecular mRNA(DEFT) and STM-2 were down regulated.CONCLUSION: Disoprofol can protect the brain and its mechanism might be related to the down regulation of three apoptosis associated genes including APAF1, DEFT and STM-2.
