中国医师进修杂志
中國醫師進脩雜誌
중국의사진수잡지
CHINESE JOURNAL OF POSTGRADUATES OF MEDICINE
2014年
32期
10-12
,共3页
胡火军%黄益玲%汪雷%王雄伟%郭金满%马金阳
鬍火軍%黃益玲%汪雷%王雄偉%郭金滿%馬金暘
호화군%황익령%왕뢰%왕웅위%곽금만%마금양
癫痫,颞叶%海马硬化%细胞凋亡%bcl-2%bax%caspase-3
癲癇,顳葉%海馬硬化%細胞凋亡%bcl-2%bax%caspase-3
전간,섭협%해마경화%세포조망%bcl-2%bax%caspase-3
Epilepsy,temporal lobe%Hippocampus sclerosis%Cell apoptosis%Bcl-2%Bax%Caspase-3
目的 探讨海马硬化型颞叶癫痫患者海马神经细胞的凋亡及凋亡相关基因的表达.方法 癫痫组为15例颞叶癫痫患者手术切除的颞叶病灶,对照组为6例脑外伤内减压术中切除的颞叶脑组织,应用HE染色、原位末端标记(TUNEL)染色及免疫组织化学染色等方法来检测神经细胞凋亡状态及凋亡相关基因bcl-2、bax及半胱氨酸蛋白酶(caspase)-3蛋白的表达.结果 对照组及癫痫组HE染色均未发现凋亡的神经细胞;TUNEL染色对照组未见阳性细胞,而癫痫组发现较多的染色阳性细胞,100个染色细胞中阳性细胞数为(4.39±2.04)个.免疫组织化学染色结果表明,对照组患者脑组织内bcl-2蛋白无表达,癫痫组15例均可见bcl-2蛋白表达明显增强[100个染色细胞中阳性细胞数为(6.72±3.36)个],两组比较差异有统计学意义(P<0.01);bax蛋白在癫痫组与对照组中均轻微表达,两组比较差异无统计学意义(P>0.05).对照组有2例检测到caspase-3蛋白的表达,而癫痫组有14例caspase-3蛋白表达明显,100个染色细胞中阳性细胞数分别为(1.07±0.43),(9.54±3.68)个,两组比较差异有统计学意义(P<0.01).结论 神经细胞凋亡是导致海马硬化的重要原因,bcl-2、caspase-3参与了这一过程并发挥了重要作用.
目的 探討海馬硬化型顳葉癲癇患者海馬神經細胞的凋亡及凋亡相關基因的錶達.方法 癲癇組為15例顳葉癲癇患者手術切除的顳葉病竈,對照組為6例腦外傷內減壓術中切除的顳葉腦組織,應用HE染色、原位末耑標記(TUNEL)染色及免疫組織化學染色等方法來檢測神經細胞凋亡狀態及凋亡相關基因bcl-2、bax及半胱氨痠蛋白酶(caspase)-3蛋白的錶達.結果 對照組及癲癇組HE染色均未髮現凋亡的神經細胞;TUNEL染色對照組未見暘性細胞,而癲癇組髮現較多的染色暘性細胞,100箇染色細胞中暘性細胞數為(4.39±2.04)箇.免疫組織化學染色結果錶明,對照組患者腦組織內bcl-2蛋白無錶達,癲癇組15例均可見bcl-2蛋白錶達明顯增彊[100箇染色細胞中暘性細胞數為(6.72±3.36)箇],兩組比較差異有統計學意義(P<0.01);bax蛋白在癲癇組與對照組中均輕微錶達,兩組比較差異無統計學意義(P>0.05).對照組有2例檢測到caspase-3蛋白的錶達,而癲癇組有14例caspase-3蛋白錶達明顯,100箇染色細胞中暘性細胞數分彆為(1.07±0.43),(9.54±3.68)箇,兩組比較差異有統計學意義(P<0.01).結論 神經細胞凋亡是導緻海馬硬化的重要原因,bcl-2、caspase-3參與瞭這一過程併髮揮瞭重要作用.
목적 탐토해마경화형섭협전간환자해마신경세포적조망급조망상관기인적표체.방법 전간조위15례섭협전간환자수술절제적섭협병조,대조조위6례뇌외상내감압술중절제적섭협뇌조직,응용HE염색、원위말단표기(TUNEL)염색급면역조직화학염색등방법래검측신경세포조망상태급조망상관기인bcl-2、bax급반광안산단백매(caspase)-3단백적표체.결과 대조조급전간조HE염색균미발현조망적신경세포;TUNEL염색대조조미견양성세포,이전간조발현교다적염색양성세포,100개염색세포중양성세포수위(4.39±2.04)개.면역조직화학염색결과표명,대조조환자뇌조직내bcl-2단백무표체,전간조15례균가견bcl-2단백표체명현증강[100개염색세포중양성세포수위(6.72±3.36)개],량조비교차이유통계학의의(P<0.01);bax단백재전간조여대조조중균경미표체,량조비교차이무통계학의의(P>0.05).대조조유2례검측도caspase-3단백적표체,이전간조유14례caspase-3단백표체명현,100개염색세포중양성세포수분별위(1.07±0.43),(9.54±3.68)개,량조비교차이유통계학의의(P<0.01).결론 신경세포조망시도치해마경화적중요원인,bcl-2、caspase-3삼여료저일과정병발휘료중요작용.
Objective To explore the role and expression of cell apoptosis regulatory genes in patients with temporal lobe epilepsy characterized by hippocampus sclerosis.Methods The experimental specimens were obtained from 15 patients with temporal lobe epilepsy (epilepsy group) and 6 control samples (control group) were obtained from temporal lobe excision of brain trauma decompression,investigated neuron apoptosis by HE stain,TdT-mediated dUTP-biotin nick end labeling (TUNEL) method,and determined the expression of bcl-2,bax and caspase-3 by immunohistochemistry.Results The evidence of neuron apoptosis was not found by HE stain in both control group and epilepsy group.Positive cells was not found in control group,but was obviously observed in epilepsy group by TUNEL staining [(4.39 ± 2.04) numbers/100].Unlike that in normal adult brain,bcl-2 immunoreactivity was obviously observed in some neurons in epilepsy group[(6.72 ± 3.36) numbers/100] (P < 0.01).Compared with control group,bax protein in epilepsy group was mild expression (P > 0.05).Two cases in control group were detected the expression of caspase-3 protein,and caspase-3 significantly increased in epilepsy group [(1.07 ± 0.43),(9.54 ± 3.68) numbers/100] (P < 0.01).Conclusions Neuron apoptosis is an important cause of hippocampal sclerosis of human epilepsy.bcl-2 and caspase-3 may play an important role in this process.