中国伤残医学
中國傷殘醫學
중국상잔의학
CHINESE JOURNAL OF TRAUMA AND DISABILITY MEDICINE
2013年
7期
97-99
,共3页
缺氧缺血性脑病%神经干细胞%干预%大鼠%动物%实验
缺氧缺血性腦病%神經榦細胞%榦預%大鼠%動物%實驗
결양결혈성뇌병%신경간세포%간예%대서%동물%실험
HIBD(Hypoxic-ischemic brain injury)%NSCs (neural stem cells)%Intervention%Rat%Animal experiment
目的：研究早期干预对缺氧缺血性脑损伤（ Hypoxic-ischemic brain injury ）新生大鼠内源性神经干细胞分化能力的影响。方法：共75只7日龄SD（ Sprague Dawley ）大鼠，随机分成模型组（ n＝50）和假手术组（ n＝25），模型组用Rice法制作50只缺氧缺血性脑病模型，分成HIBD组（n＝25）和干预组（n＝25）。对干预组进行早期干预，HIBD组和假手术组常规饲养，每组选取1天，7天，14天，21天，28天5个时间点处死5只，每只鼠处死前都进行腹腔BrdU注射标记新生细胞，应用荧光免疫双标技术检测各时间点海马齿状（DG）GFAP/BrdU和NeuN/BrdU阳性细胞数。结果：（1）3组大鼠DG区均有BrdU/NeuN和BrdU/GFAP阳性双标记染色；（2）与假手术组比较，干预组及HIBD组大鼠DG区BrdU/NeuN和BrdU/GFAP阳性双标记染色在术后14，21，28天均有显著增高（P＜0．01）。（3）早期干预组大鼠术后14，21，28天时的BrdU/NeuN和BrdU/GFAP阳性双标记染色均显著高于HIBD组（P＜0．01）。结论：缺氧缺血致大鼠脑损伤可诱导内源性神经干细胞分化；早期干预可提高脑损伤鼠内源性神经干细胞分化能力。
目的：研究早期榦預對缺氧缺血性腦損傷（ Hypoxic-ischemic brain injury ）新生大鼠內源性神經榦細胞分化能力的影響。方法：共75隻7日齡SD（ Sprague Dawley ）大鼠，隨機分成模型組（ n＝50）和假手術組（ n＝25），模型組用Rice法製作50隻缺氧缺血性腦病模型，分成HIBD組（n＝25）和榦預組（n＝25）。對榦預組進行早期榦預，HIBD組和假手術組常規飼養，每組選取1天，7天，14天，21天，28天5箇時間點處死5隻，每隻鼠處死前都進行腹腔BrdU註射標記新生細胞，應用熒光免疫雙標技術檢測各時間點海馬齒狀（DG）GFAP/BrdU和NeuN/BrdU暘性細胞數。結果：（1）3組大鼠DG區均有BrdU/NeuN和BrdU/GFAP暘性雙標記染色；（2）與假手術組比較，榦預組及HIBD組大鼠DG區BrdU/NeuN和BrdU/GFAP暘性雙標記染色在術後14，21，28天均有顯著增高（P＜0．01）。（3）早期榦預組大鼠術後14，21，28天時的BrdU/NeuN和BrdU/GFAP暘性雙標記染色均顯著高于HIBD組（P＜0．01）。結論：缺氧缺血緻大鼠腦損傷可誘導內源性神經榦細胞分化；早期榦預可提高腦損傷鼠內源性神經榦細胞分化能力。
목적：연구조기간예대결양결혈성뇌손상（ Hypoxic-ischemic brain injury ）신생대서내원성신경간세포분화능력적영향。방법：공75지7일령SD（ Sprague Dawley ）대서，수궤분성모형조（ n＝50）화가수술조（ n＝25），모형조용Rice법제작50지결양결혈성뇌병모형，분성HIBD조（n＝25）화간예조（n＝25）。대간예조진행조기간예，HIBD조화가수술조상규사양，매조선취1천，7천，14천，21천，28천5개시간점처사5지，매지서처사전도진행복강BrdU주사표기신생세포，응용형광면역쌍표기술검측각시간점해마치상（DG）GFAP/BrdU화NeuN/BrdU양성세포수。결과：（1）3조대서DG구균유BrdU/NeuN화BrdU/GFAP양성쌍표기염색；（2）여가수술조비교，간예조급HIBD조대서DG구BrdU/NeuN화BrdU/GFAP양성쌍표기염색재술후14，21，28천균유현저증고（P＜0．01）。（3）조기간예조대서술후14，21，28천시적BrdU/NeuN화BrdU/GFAP양성쌍표기염색균현저고우HIBD조（P＜0．01）。결론：결양결혈치대서뇌손상가유도내원성신경간세포분화；조기간예가제고뇌손상서내원성신경간세포분화능력。
Objective:To study the impact of early intervention on differentiation of neural stem cells ( NSCs) in brain damage rats af-ter HIBD(Hypoxic-ischemic brain injury).Methods:Totally 75 SD(Sprague Dawley)rats aged 7 days were randomly divided into two groups:HIBD model(n=50)and sham-operated(n=25).50 HIBD model was produced with Rice method ,and randomly divided into HIBD group(n=25) and early intervention group(n=25).HIBD group and sham-operated group are normally feed, intervention group are dealed with early intervention ,5 rats were killed at 1day,7days,14days,21days and 28days after operation in each group .Each rat was injected with BrdU into its abdominal cavity to mark new cells before killed .Double staining immunofluorescence was used to detect the co-expression of bromodeoxyuridine (BrdU) with neuronal nuclei antigen (NeuN) or glia fibrillary acidic protein (GFAP) in the Dentate gyrus(DG) at different time points.Results:(1)BrdU/NeuN and BrdU/GFAP double staining cells were observed in all 3 groups.(2) In the HIBD and intervention groups , at 14、21 and 28 days after the surgery , the number of BrdU/NeuN and BrdU/GFAP double -stained cells increased in the DG compared with the sham -operated group(P<0.01).(3)Obviously more BrdU/NeuN and BrdU/GFAP double-stained cells were found in the early intervention group than that in the HIBD group at 14, 21 and 28days(P<0.01).Conclu-sion:Our results indicate that the brain damae caused by HIBD can induce the differentiation of endogenous NSCs ;Early intervention can increase the differentiation of endogenous NSCs .
