中华医学杂志
中華醫學雜誌
중화의학잡지
National Medical Journal of China
2009年
43期
3058-3060
,共3页
姚丽芬%王真奎%王真刚%隋丹%张黎明
姚麗芬%王真奎%王真剛%隋丹%張黎明
요려분%왕진규%왕진강%수단%장려명
癫痫%颞叶%免疫组织化学
癲癇%顳葉%免疫組織化學
전간%섭협%면역조직화학
Epilepsy,temporal lobe%Immunohistochemistry
目的 探讨缝隙连接蛋白Cx32、Cx43在难治性颞叶癫痫患者病变海马组织中的表达及缝隙连接与难治性颞叶癫痫患者癫痫发作的关系.方法 实验组为14例难治颞叶癫痫(伴海马硬化)患者手术切除的病变海马组织,对照组为8例因其他非颅内疾病死亡进行尸体解剖者的正常海马组织,死者生前无癫痫发作,利用免疫组织化学与蛋白印迹检测方法检测两组间缝隙连接蛋白Cx32和Cx43的表达,并进行比较.结果 应用免疫组织化学方法发现连接蛋白在对照组中有比较低的水平表达[Cx32阳性细胞个数为(9.4±1.1);Cx43阳性细胞个数为(9.2±4.7)],但在癫痫患者的海马组织中表达增强[Cx32阳性细胞个数为(14.6±3.4);Cx43阳性细胞个数为(16.5±3.1)],差异均有统计学意义(P<0.01);通过蛋白印迹检测方法发现连接蛋白在对照组中也有低水平表达[Cx32灰度比值为(0.2±0.1);Cx43灰度比值为(0.5±0.2)],在癫痫患者的海马组织中表达明显增强[Cx32灰度比值为(1.5±0.2);Cx43灰度比值为(1.4±0.3)],差异均有统计学意义(均P<0.01).结论 难治性颢叶癫痫患者海马脑组织中缝隙连接蛋白Cx32、Cx43表达增高,缝隙连接蛋白在难治性癫痫的发生、发展过程中可能起到了重要作用.
目的 探討縫隙連接蛋白Cx32、Cx43在難治性顳葉癲癇患者病變海馬組織中的錶達及縫隙連接與難治性顳葉癲癇患者癲癇髮作的關繫.方法 實驗組為14例難治顳葉癲癇(伴海馬硬化)患者手術切除的病變海馬組織,對照組為8例因其他非顱內疾病死亡進行尸體解剖者的正常海馬組織,死者生前無癲癇髮作,利用免疫組織化學與蛋白印跡檢測方法檢測兩組間縫隙連接蛋白Cx32和Cx43的錶達,併進行比較.結果 應用免疫組織化學方法髮現連接蛋白在對照組中有比較低的水平錶達[Cx32暘性細胞箇數為(9.4±1.1);Cx43暘性細胞箇數為(9.2±4.7)],但在癲癇患者的海馬組織中錶達增彊[Cx32暘性細胞箇數為(14.6±3.4);Cx43暘性細胞箇數為(16.5±3.1)],差異均有統計學意義(P<0.01);通過蛋白印跡檢測方法髮現連接蛋白在對照組中也有低水平錶達[Cx32灰度比值為(0.2±0.1);Cx43灰度比值為(0.5±0.2)],在癲癇患者的海馬組織中錶達明顯增彊[Cx32灰度比值為(1.5±0.2);Cx43灰度比值為(1.4±0.3)],差異均有統計學意義(均P<0.01).結論 難治性顥葉癲癇患者海馬腦組織中縫隙連接蛋白Cx32、Cx43錶達增高,縫隙連接蛋白在難治性癲癇的髮生、髮展過程中可能起到瞭重要作用.
목적 탐토봉극련접단백Cx32、Cx43재난치성섭협전간환자병변해마조직중적표체급봉극련접여난치성섭협전간환자전간발작적관계.방법 실험조위14례난치섭협전간(반해마경화)환자수술절제적병변해마조직,대조조위8례인기타비로내질병사망진행시체해부자적정상해마조직,사자생전무전간발작,이용면역조직화학여단백인적검측방법검측량조간봉극련접단백Cx32화Cx43적표체,병진행비교.결과 응용면역조직화학방법발현련접단백재대조조중유비교저적수평표체[Cx32양성세포개수위(9.4±1.1);Cx43양성세포개수위(9.2±4.7)],단재전간환자적해마조직중표체증강[Cx32양성세포개수위(14.6±3.4);Cx43양성세포개수위(16.5±3.1)],차이균유통계학의의(P<0.01);통과단백인적검측방법발현련접단백재대조조중야유저수평표체[Cx32회도비치위(0.2±0.1);Cx43회도비치위(0.5±0.2)],재전간환자적해마조직중표체명현증강[Cx32회도비치위(1.5±0.2);Cx43회도비치위(1.4±0.3)],차이균유통계학의의(균P<0.01).결론 난치성호협전간환자해마뇌조직중봉극련접단백Cx32、Cx43표체증고,봉극련접단백재난치성전간적발생、발전과정중가능기도료중요작용.
Objective To study the expression of Cx32 and Cx43 in medically intractable temporal lobe epilepsy in human and investigate the pathogenic relationship between gap junctions and seizures. Methods The expression of Cx32 and Cx43 was detected by Western blot and immunohistochemistry in 14 consecutive samples of hippocampus from epileptic patients undergoing an amygdalohippocampectomy for the treatment of intractable seizures. During postmortem dissection, 8 samples of hippocampus in nonepileptic patients dying of other diseases were taken as control group. Results The expression of Cx32 and Cx43 was at a low level in the control group [Cx32 : count of positive cell (9.4± 1.1), ratios of gray scale (0.2±0.1) ; Cx43 : count of positive cell (9.2±4.7), ratios of gray scale (0.5±0.2)], but Cx43 and Cx32 appeared to be expressed at a higher level in epileptic patients compared with that of the control group by immunohistochemistry [Cx32 : count of positive cell (14.6±3.4), Cx43:count of positive cell (16.5±3.1) ] (P<0.01), and their expression significantly increased by Western blot [Cx32 : ratios of gray scale (1.5±0.2), Cx43 : ratios of gray scale (1.4±0.3)] (P<0.01). Over-expression of Cx32 and Cx43 was found in 14 consecutive samples of hippocampus from epileptic patients. Conclusion Gap junctions play an important role in the occurrence and progression of intractable seizures.