〔 摘要〕　 目的 　 研究早期干預(yù)對缺氧缺血性腦損傷 ( HIBD) 大鼠學(xué)習(xí)記憶功能的影響及其作用機制。方法 　選用
SD大鼠建立宮內(nèi) HIBD動物模型 , 隨機分為非干預(yù)組和干預(yù)組 , 非干預(yù)組與正常對照組常規(guī)飼養(yǎng) , 對干預(yù)組采取早期觸摸
和豐富環(huán)境刺激。干預(yù) 28d后 , 通過三等臂 Y型迷宮試驗檢測各組大鼠的學(xué)習(xí)記憶功能 , 而后取大鼠額皮質(zhì)和海馬組織進
行病理觀察 , 并采用DNA 缺口原位末端標記法 ( TUNEL 反應(yīng)法) 檢測凋亡細胞 , 觀察腦組織神經(jīng)元凋亡情況。結(jié)果 　單
純 HIBD組大鼠學(xué)習(xí)獲得與記憶保持能力明顯低于正常對照組 ( P < 0101) , 但 HIBD 干預(yù)組 Y迷宮測試成績則優(yōu)于 HIBD
非干預(yù)組 ( P < 0101) 。同時 , HIBD非干預(yù)組腦額皮質(zhì)和海馬 CA1 區(qū)神經(jīng)元缺失遠較正常組多 ( P < 0101) , 而 HIBD 干預(yù)
組與 HIBD 非干預(yù)組之間神經(jīng)元數(shù)量的差異則不那么顯著。但 HIBD 干預(yù)組腦額皮質(zhì)和海馬神經(jīng)元凋亡百分率明顯低于
HIBD非干預(yù)組 ( P < 0101) 。結(jié)論 　早期干預(yù)可減輕缺氧缺血性損傷腦組織神經(jīng)細胞凋亡 , 該作用可能是早期干預(yù)促進
HIBD大鼠腦功能修復(fù)的機制之一。
〔 關(guān)鍵詞〕　 缺氧缺血性腦損傷; 　 早期干預(yù); 　 大鼠; 　 學(xué)習(xí)記憶; 　 神經(jīng)元; 　 凋亡
〔 中圖分類號〕　R74311 　　〔 文獻標識碼〕　A
CHANGES OF APOPTOTIC NEURONS IN THE BRAIN OF NEONATAL RATS AFTER
HYPOXIA2ISCHEMIA AND EARLY INTERVENTION
Chen Min , Chen Minrong1
, Chen Yuanhui
1
, Chen Daguang1
( Dep artment of Medical L aboratory , Medical Technolog y and Engi neeri n g Col lege ,
Fuj i an Medical Uni versi t y , Fuz hou 350004 , Chi na)
〔 Abstract〕　Objective To explore t he effect of early intervention on f unctional outcome and neuron
apopto sis in t he brain of rat s wit h hypoxic2ischemic brain damage ( HIBD) . Methods SD rat s were used to
establish the model of HIBD. The HIBD rat s were randomly divide into two group s : non2intervention
group and intervention group t hat received t he neonatal handling and was kept in an enriched environ2
ment . Non2intervention group and normal cont rol group were kept in a standard condition. On t he 28t h
days af ter t he operation , the learning2memory ability of rat s in every group was evaluated t hrouth t ri2e2
qual2arm maze test . Terminal deoxynucleotidyl t ransferase2mediated dTUP biotinylated nick end labeling
( TUNEL) met hod was used to detect neuron apopto sis in pref rontal cortex and hippocamp us of rat s. Re2
sult s Compared wit h the normal group , the non2intervention HIBD group was significant ly decreased in t he
Y2maze learning ability ( P < 0101) , while t he learning2memory ability of t he intervention HIBD group
was obviously improved ( P < 0101) . The pat hology differentiation was obvious between the HIBD
group s and the normal cont rol s. The p ref rontal cortex and hippocampal CA1 neurons of t he HIBD group s
were apparently decreased in number as compared with those of t he normal cont rol s ( P < 0101) , while t he
neurons of t he HIBD intervention group were a lit t le more than those of t he HIBD non2intervention group .
At t he same time , t he percentage of TUNEL positive neurons in pref rontal cortex and hippocamp us of t he
intervention group was less t han t hat of t he non2intervention group ( P < 0101) . Conclusion Early interven2
tion can decrease t he percentage of apoptotic neurons in t he brain of rat s wit h HIBD , which may be one of
t he mechanisms of early intervention improving t he f unctional outcome of HIBD rat s.
〔Key words〕　Hypoxic2ischemic brain damage ; 　Early intervention ; 　Rat ; 　Learning2memory ;
　Neuron ; 　Apoptosis