中国小儿急救医学
中國小兒急救醫學
중국소인급구의학
CHINESE PEDIATRIC EMERGENCY MEDICINE
2008年
5期
451-454
,共4页
脑白质损伤%宫内感染%大鼠%细胞凋亡%Bcl-2%Bax
腦白質損傷%宮內感染%大鼠%細胞凋亡%Bcl-2%Bax
뇌백질손상%궁내감염%대서%세포조망%Bcl-2%Bax
White matter damage%Intrauterine infection%Rat%Apoptosis%Bcl-2%Bax
目的 探讨内毒素致胎鼠脑白质损伤后凋亡蛋白Bcl-2、Bax的表达及其意义.方法 孕鼠随机分为两组:感染组和对照组.感染组:建立宫内感染的动物模型,孕鼠怀孕15 d腹腔注射内毒素;对照组:孕鼠怀孕15 d腹腔注射生理盐水.分别于给药后2、4、12、24、72 h剖腹取胎鼠,取脑组织行组织病理学检查,观察胎盘及胎鼠脑组织病理特点,用免疫组织化学方法检测胎鼠脑组织凋亡蛋白Bcl-2、Bax的表达.结果 感染组胎盘组织见中性粒细胞浸润,胎鼠脑组织病理改变包括脑白质染色减淡,结构疏松等.感染组胎鼠脑组织凋亡蛋白Bcl-2的表达自2 h开始逐渐下降,而Bax的表达自2 h逐渐升高,均于12h达到峰值.2h感染组Bcl-2、Bax的阳性细胞百分数与对照组相比,差异无显著性(P>0.05);而4 h、12 h、24 h和72 h感染组与对照组相比,差异有非常显著性(P<0.01).感染组Bax与Bcl-2的比值均明显高于对照组,在各观察时间点两组相比,差异有非常显著性(P<0.01).结论 内毒素诱导是制备胎鼠脑白质损伤的一种有效形式.在胎鼠脑白质损伤中Bcl-2可能抑制细胞凋亡,Bax可能诱发细胞凋亡,两者的比率变化可能对脑白质损伤后细胞凋亡的调节起重要作用.
目的 探討內毒素緻胎鼠腦白質損傷後凋亡蛋白Bcl-2、Bax的錶達及其意義.方法 孕鼠隨機分為兩組:感染組和對照組.感染組:建立宮內感染的動物模型,孕鼠懷孕15 d腹腔註射內毒素;對照組:孕鼠懷孕15 d腹腔註射生理鹽水.分彆于給藥後2、4、12、24、72 h剖腹取胎鼠,取腦組織行組織病理學檢查,觀察胎盤及胎鼠腦組織病理特點,用免疫組織化學方法檢測胎鼠腦組織凋亡蛋白Bcl-2、Bax的錶達.結果 感染組胎盤組織見中性粒細胞浸潤,胎鼠腦組織病理改變包括腦白質染色減淡,結構疏鬆等.感染組胎鼠腦組織凋亡蛋白Bcl-2的錶達自2 h開始逐漸下降,而Bax的錶達自2 h逐漸升高,均于12h達到峰值.2h感染組Bcl-2、Bax的暘性細胞百分數與對照組相比,差異無顯著性(P>0.05);而4 h、12 h、24 h和72 h感染組與對照組相比,差異有非常顯著性(P<0.01).感染組Bax與Bcl-2的比值均明顯高于對照組,在各觀察時間點兩組相比,差異有非常顯著性(P<0.01).結論 內毒素誘導是製備胎鼠腦白質損傷的一種有效形式.在胎鼠腦白質損傷中Bcl-2可能抑製細胞凋亡,Bax可能誘髮細胞凋亡,兩者的比率變化可能對腦白質損傷後細胞凋亡的調節起重要作用.
목적 탐토내독소치태서뇌백질손상후조망단백Bcl-2、Bax적표체급기의의.방법 잉서수궤분위량조:감염조화대조조.감염조:건립궁내감염적동물모형,잉서부잉15 d복강주사내독소;대조조:잉서부잉15 d복강주사생리염수.분별우급약후2、4、12、24、72 h부복취태서,취뇌조직행조직병이학검사,관찰태반급태서뇌조직병리특점,용면역조직화학방법검측태서뇌조직조망단백Bcl-2、Bax적표체.결과 감염조태반조직견중성립세포침윤,태서뇌조직병리개변포괄뇌백질염색감담,결구소송등.감염조태서뇌조직조망단백Bcl-2적표체자2 h개시축점하강,이Bax적표체자2 h축점승고,균우12h체도봉치.2h감염조Bcl-2、Bax적양성세포백분수여대조조상비,차이무현저성(P>0.05);이4 h、12 h、24 h화72 h감염조여대조조상비,차이유비상현저성(P<0.01).감염조Bax여Bcl-2적비치균명현고우대조조,재각관찰시간점량조상비,차이유비상현저성(P<0.01).결론 내독소유도시제비태서뇌백질손상적일충유효형식.재태서뇌백질손상중Bcl-2가능억제세포조망,Bax가능유발세포조망,량자적비솔변화가능대뇌백질손상후세포조망적조절기중요작용.
Objective To investigate the changes of Bcl-2 and Bax expression in white matter of fetal rats after maternal endotoxin administration. Methods Pregnant rats were randomly divided into two groups: infection group and control group. The infection group was established by intraperitoneal injection of endotoxin in pregnant rats when gestation was 70% complete (15 days). The control group was treated with normal saline. The fetal rats were killed at 2, 4, 12, 24 and 72 hours after maternal endotoxin administration. The pathological changes in placenta and in fetal rat brain were determined by HE staining. Immunohistochemical method was used to detect the expression of Bcl-2 and Bax proteins in fetal rat brains. Results The major pathological changes in fetal rats niter maternal endotoxin administration included neutrophil infiltration in the placenta, weak staining of white matter and focal infarction. After maternal endotoxin administration, the expression of Bcl-2 gradually decreased from 2 h and arrived at the valley at 12 h, while that of Bax gradually increased 2 h and reached a peak at 12 h. Between the endotoxin-gronp and the control group, the number of positive cells of Bcl-2 and Bax in brain of the fetal rat had significant difference at 4, 12, 24 and 72 hours (P< 0.01 ), and there was no significant difference at 2 h (P > 0.05). The ratio of Bax to Bcl-2 in the endotoxingroup was significantly higher than that in the control group at each time point (P<0.01).Conclusion Endotoxin can be used to eatablish intrauterine irfection models and the infection may cause damage to the white matter. Overexpression of Bcl-2 protects cell from apoptosis, but Bax may function as a cell death effector pro-tein. The ratio of Bax to Bcl-2 may play an important role for apoptosis in the lesion of the white matter.
