中南大学学报(医学版)
中南大學學報(醫學版)
중남대학학보(의학판)
JOURNAL OF CENTRAL SOUTH UNIVERSITY (MEDICAL SCIENCES)
2009年
6期
468-475
,共8页
彭争荣%肖平田%郭华%刘清红
彭爭榮%肖平田%郭華%劉清紅
팽쟁영%초평전%곽화%류청홍
脑缺血再灌注%高压氧%细胞凋亡%学习记忆
腦缺血再灌註%高壓氧%細胞凋亡%學習記憶
뇌결혈재관주%고압양%세포조망%학습기억
cerebral ischemia-reperfusion%hyperbaric oxygen%apoptosis%learning and memory
目的:探讨早期高压氧(脑缺血再灌注30 min后)对脑缺血再灌注神经细胞凋亡及学习与记忆的影响.方法:将实验用大鼠随机分为假手术组、模型组及处理组.采用Zea Longa法制作脑缺血再灌注动物模型,观察大鼠早期高压氧处理后神经功能缺损评分、海马区凋亡阳性细胞计数、caspase-3和Bcl-2蛋白表达的改变情况;并采用Morris水迷宫检测大鼠的逃避潜伏期(EL)和穿过原平台次数的变化.结果:第2 h, 1 d, 2 d, 3 d大鼠神经功能缺损评分模型组和处理组均较假手术组增加(P<0.01),第2, 3 d大鼠神经功能缺损评分处理组较模型组明显降低(P<0.05);模型组凋亡细胞计数和caspase-3蛋白表达量显著多于假手术组(P<0.01),而处理组较模型组明显减少(P<0.01);模型组Bcl-2蛋白量较假手术组明显增加(P<0.01),处理组则更高于模型组(P<0.01);模型组EL时间比假手术组明显延长,穿过原平台次数明显少于假手术组(P<0.01),而处理组EL时间则较模型组明显缩短,穿过原平台次数则明显多于模型组(P<0.05).结论:早期高压氧能抑制脑缺血再灌注损伤海马神经细胞的凋亡,提高学习记忆功能.
目的:探討早期高壓氧(腦缺血再灌註30 min後)對腦缺血再灌註神經細胞凋亡及學習與記憶的影響.方法:將實驗用大鼠隨機分為假手術組、模型組及處理組.採用Zea Longa法製作腦缺血再灌註動物模型,觀察大鼠早期高壓氧處理後神經功能缺損評分、海馬區凋亡暘性細胞計數、caspase-3和Bcl-2蛋白錶達的改變情況;併採用Morris水迷宮檢測大鼠的逃避潛伏期(EL)和穿過原平檯次數的變化.結果:第2 h, 1 d, 2 d, 3 d大鼠神經功能缺損評分模型組和處理組均較假手術組增加(P<0.01),第2, 3 d大鼠神經功能缺損評分處理組較模型組明顯降低(P<0.05);模型組凋亡細胞計數和caspase-3蛋白錶達量顯著多于假手術組(P<0.01),而處理組較模型組明顯減少(P<0.01);模型組Bcl-2蛋白量較假手術組明顯增加(P<0.01),處理組則更高于模型組(P<0.01);模型組EL時間比假手術組明顯延長,穿過原平檯次數明顯少于假手術組(P<0.01),而處理組EL時間則較模型組明顯縮短,穿過原平檯次數則明顯多于模型組(P<0.05).結論:早期高壓氧能抑製腦缺血再灌註損傷海馬神經細胞的凋亡,提高學習記憶功能.
목적:탐토조기고압양(뇌결혈재관주30 min후)대뇌결혈재관주신경세포조망급학습여기억적영향.방법:장실험용대서수궤분위가수술조、모형조급처리조.채용Zea Longa법제작뇌결혈재관주동물모형,관찰대서조기고압양처리후신경공능결손평분、해마구조망양성세포계수、caspase-3화Bcl-2단백표체적개변정황;병채용Morris수미궁검측대서적도피잠복기(EL)화천과원평태차수적변화.결과:제2 h, 1 d, 2 d, 3 d대서신경공능결손평분모형조화처리조균교가수술조증가(P<0.01),제2, 3 d대서신경공능결손평분처리조교모형조명현강저(P<0.05);모형조조망세포계수화caspase-3단백표체량현저다우가수술조(P<0.01),이처리조교모형조명현감소(P<0.01);모형조Bcl-2단백량교가수술조명현증가(P<0.01),처리조칙경고우모형조(P<0.01);모형조EL시간비가수술조명현연장,천과원평태차수명현소우가수술조(P<0.01),이처리조EL시간칙교모형조명현축단,천과원평태차수칙명현다우모형조(P<0.05).결론:조기고압양능억제뇌결혈재관주손상해마신경세포적조망,제고학습기억공능.
Objective To explore the effect of early hyperbaric oxygen (HBO) on neuronal apoptosis and learning and memory in rats treated with cerebral ischemia-reperfusion injury in 30 min.Methods Experimental rats were randomly divided into 3 groups: a sham-operation group, a model group, and a treatment group. Cerebral ischemia-reperfusion injury model was induced by Zea Longa's method. Neurologic impairment score, apoptosis cell, and the expression of caspase-3 and Bcl-2 protein were observed. The amount across platform and the escape latency (EL) time were determined by Morris water maze.Results Neurologic impairment scores at 2 h, 1 d, 2 d, and 3 d of the model group and the treatment group were obviously higher than the sham-operation group (P<0.01), and those at 2 d and 3 d of the treatment group were obviously lower than those of the model group (P<0.05). The number of apoptosis cells and the expression of caspase-3 protein in the model group significantly increased compared with those in the sham-operation group (P<0.01), while those in the treatment group was significantly lower than the model group (P<0.01). Bcl-2 protein expression in the model group increased more obviously than that in the sham-operation group (P<0.01), and that in the treatment group was much higher than the model group (P<0.01). The EL time of the model group was much longer than that of the sham-operation group and the number across platform was obviously decreased compared with that of the sham-operation group (P<0.01), while the EL time of the treatment group was much shorter than that of the model group and the number across platform was more than that of the model group (P<0.05).Conclusion Early hyperbaric oxygen could inhibit nerve cell apoptosis suffered cerebral ischemia-reperfusion injury and improve the function of learning and memory.