中国临床康复
中國臨床康複
중국림상강복
CHINESE JOURNAL OF CLINICAL REHABILITATION
2005年
5期
205-207
,共3页
吴春燕%彭晓晖%穆莉芳%赵红丽%张爱启%胡孟英
吳春燕%彭曉暉%穆莉芳%趙紅麗%張愛啟%鬍孟英
오춘연%팽효휘%목리방%조홍려%장애계%호맹영
癫痫%基因,bcl-2%2-氯腺苷%大鼠%受体,嘌呤能P1
癲癇%基因,bcl-2%2-氯腺苷%大鼠%受體,嘌呤能P1
전간%기인,bcl-2%2-록선감%대서%수체,표령능P1
背景:癫痫发作后大脑海马神经元有明显受损,而癫痫后神经细胞损害有坏死和凋亡两种形式,在癫痫神经损害中起着重要作用.腺苷作为内源性神经保护递质,可以抑制兴奋性氨基酸的释放、氧自由基的产生以及一氧化氮的作用,同时还有改善脑血流以及抗惊厥作用.但有关腺苷与癫痫后细胞凋亡之间的关系尚不完全清楚.目的:观察腺苷受体激动剂2-CAdo对癫痫大鼠海马神经细胞bcl-2,Bax基因表达的影响,进一步探讨腺苷抗惊厥及脑保护的作用机制.设计:以实验动物为研究对象,完全随机对照实验研究.单位:一所油田总医院的儿科和普外科,一所大学医院儿内科.材料:实验于2002-10/2003-03在哈尔滨医科大学实验动物学部及病理教研室完成.体质量200～250 g健康成年Wistar大鼠104只,雌雄各半.动物随机分为正常组8只,致痫组32只,致痫+2-CAdo组32只,致痫+生理盐水组32只.干预:按1.5 mg/kg腹腔注射马桑内酯(由哈尔滨医科大学药理学部提供)建立动物癫痫模型,全部大鼠于注射后5 min出现抽搐,持续时间一两分钟.致痫+2-CAdo组于马桑内酯注射前1 h及抽搐后1 h经尾静脉注射2-CAdo(由ICN公司提供)剂量为0.6 mg/kg,致痫+生理盐水组于马桑内酯注射前1 h及抽搐后1 h经尾静脉注射等量的生理盐水.主要观察指标:海马CA1区bcl-2,Bax基因表达阳性细胞数.结果:癫痫发作后24 h海马CA1区神经细胞bcl-2表达量增多,48 h明显下降,72 h仅有少量表达,7 d时其表达量再度升高.而Bax表达则在癫痫发作24 h开始增多,48 h显著增多,72 h表达达高峰,7 d表达量最少.致痫+2-CAdo组各相应时间点bcl-2表达量较致痫组、致痫+生理盐水组明显增高(P＜0 05),Bax表达量较致痫组、致痫+生理盐水组明显减少(P＜0.05),有统计学意义.结论:2-CAdo能够减少癫痫发作后海马神经细胞的凋亡,对神经细胞有一定的保护作用.
揹景:癲癇髮作後大腦海馬神經元有明顯受損,而癲癇後神經細胞損害有壞死和凋亡兩種形式,在癲癇神經損害中起著重要作用.腺苷作為內源性神經保護遞質,可以抑製興奮性氨基痠的釋放、氧自由基的產生以及一氧化氮的作用,同時還有改善腦血流以及抗驚厥作用.但有關腺苷與癲癇後細胞凋亡之間的關繫尚不完全清楚.目的:觀察腺苷受體激動劑2-CAdo對癲癇大鼠海馬神經細胞bcl-2,Bax基因錶達的影響,進一步探討腺苷抗驚厥及腦保護的作用機製.設計:以實驗動物為研究對象,完全隨機對照實驗研究.單位:一所油田總醫院的兒科和普外科,一所大學醫院兒內科.材料:實驗于2002-10/2003-03在哈爾濱醫科大學實驗動物學部及病理教研室完成.體質量200～250 g健康成年Wistar大鼠104隻,雌雄各半.動物隨機分為正常組8隻,緻癇組32隻,緻癇+2-CAdo組32隻,緻癇+生理鹽水組32隻.榦預:按1.5 mg/kg腹腔註射馬桑內酯(由哈爾濱醫科大學藥理學部提供)建立動物癲癇模型,全部大鼠于註射後5 min齣現抽搐,持續時間一兩分鐘.緻癇+2-CAdo組于馬桑內酯註射前1 h及抽搐後1 h經尾靜脈註射2-CAdo(由ICN公司提供)劑量為0.6 mg/kg,緻癇+生理鹽水組于馬桑內酯註射前1 h及抽搐後1 h經尾靜脈註射等量的生理鹽水.主要觀察指標:海馬CA1區bcl-2,Bax基因錶達暘性細胞數.結果:癲癇髮作後24 h海馬CA1區神經細胞bcl-2錶達量增多,48 h明顯下降,72 h僅有少量錶達,7 d時其錶達量再度升高.而Bax錶達則在癲癇髮作24 h開始增多,48 h顯著增多,72 h錶達達高峰,7 d錶達量最少.緻癇+2-CAdo組各相應時間點bcl-2錶達量較緻癇組、緻癇+生理鹽水組明顯增高(P＜0 05),Bax錶達量較緻癇組、緻癇+生理鹽水組明顯減少(P＜0.05),有統計學意義.結論:2-CAdo能夠減少癲癇髮作後海馬神經細胞的凋亡,對神經細胞有一定的保護作用.
배경:전간발작후대뇌해마신경원유명현수손,이전간후신경세포손해유배사화조망량충형식,재전간신경손해중기착중요작용.선감작위내원성신경보호체질,가이억제흥강성안기산적석방、양자유기적산생이급일양화담적작용,동시환유개선뇌혈류이급항량궐작용.단유관선감여전간후세포조망지간적관계상불완전청초.목적:관찰선감수체격동제2-CAdo대전간대서해마신경세포bcl-2,Bax기인표체적영향,진일보탐토선감항량궐급뇌보호적작용궤제.설계:이실험동물위연구대상,완전수궤대조실험연구.단위:일소유전총의원적인과화보외과,일소대학의원인내과.재료:실험우2002-10/2003-03재합이빈의과대학실험동물학부급병리교연실완성.체질량200～250 g건강성년Wistar대서104지,자웅각반.동물수궤분위정상조8지,치간조32지,치간+2-CAdo조32지,치간+생리염수조32지.간예:안1.5 mg/kg복강주사마상내지(유합이빈의과대학약이학부제공)건립동물전간모형,전부대서우주사후5 min출현추휵,지속시간일량분종.치간+2-CAdo조우마상내지주사전1 h급추휵후1 h경미정맥주사2-CAdo(유ICN공사제공)제량위0.6 mg/kg,치간+생리염수조우마상내지주사전1 h급추휵후1 h경미정맥주사등량적생리염수.주요관찰지표:해마CA1구bcl-2,Bax기인표체양성세포수.결과:전간발작후24 h해마CA1구신경세포bcl-2표체량증다,48 h명현하강,72 h부유소량표체,7 d시기표체량재도승고.이Bax표체칙재전간발작24 h개시증다,48 h현저증다,72 h표체체고봉,7 d표체량최소.치간+2-CAdo조각상응시간점bcl-2표체량교치간조、치간+생리염수조명현증고(P＜0 05),Bax표체량교치간조、치간+생리염수조명현감소(P＜0.05),유통계학의의.결론:2-CAdo능구감소전간발작후해마신경세포적조망,대신경세포유일정적보호작용.
BACKGROUND: Hippocampal neuron presents remarkably injury in cerebral after seizure of epilepsy. Necrosis and apoptosis are two kinds of neural cell injury after epilepsy and play an important role in neural injury of epilepsy. Being endogenous neural protective transmitter, adenosine may inhibit the release of excitatory amino acid, production of oxygenic free radical and action of nitric oxide. Simultaneously, it can improve cerebral blood flow and anti-convulsion. But it has been unknown concerning to the relationship between adenosine and cell apoptosis after epilepsy yet.OBJECTIVE: To observe the effects of 2-CAdo adenosine-receptor excitant on genetic expression of bcl-2, Bax of hippocampal cells in epileptic rats and further probe into the mechanism of adenosine on anti-convulsion and brain protection.DESIGN: Completely randomized controlled experimental research in which the experimental animals were taken as the objects.SETTING: Pediatrics department and general surgical department of one oil field general hospital, and pediatric internal department of a hospital affiliated to one university.MATERIALS: The experiment was performed in Experimental Zoology Departnent and Pathological Teaching & Research Department of Harbin Medical University from October 2002 to March 2003. Totally 104 Wistar rats of either sex were employed, weighing varied from 200 g to 250 g. The animals were randomly divided, named as normal group 8 rats, epileptic group 32 rats, epileptic & 2-CAdo group 32 rats, and epileptic & physiological saline group 32 rats.INTERVENTIONS: The animal epileptic model was set up by intra-abdominal injection of coriamyrtin 15 mg/kg(provided by Pathology Department of Harbin Medical University. Convulsion presented in all of rats, 5 minutes later after injection, lasting for 1 or 2 minutes. In epileptic & 2-CAdo group, 2-CAdo(provided by ICN company), 0.6 mg/kg, was injected from the vein on the tail 1 hour before coriamyrtin injection and 1 hour after convulsion respectively. In epileptic & physiological saline group, the physiological saline of equal dosage was injected from the vein on the tail 1 hour before coriamyrtin injection and 1 hour after convulsion respectively.MAIN OUTCOME MEASURES: Positive cell counts of bcl-2 and Bax genetic expression in hippocampal CA1 area.RESULTS: Twenty-four hours after epilepsy seizure, neural cell bcl-2 expression was increased in hippocampal CA1 area, was remarkably decreased in 48 hours, and the expression was only little amount in 72 hours, but it was increased again in 7 days. Bax expression began increased in 24 hours after epilepsy seizure, was significantly increased in 48 hours, reached the peak in 72 hours, the expression was the minimum in 7 days. In epileptic & 2-CAdo group, bcl-2 expressions at corresponding times were remarkably increased compared with epileptic group and epileptic & physiological saline group( P＜ 0.05), Bax expressions were remarkably decreased compared with epileptic group and epileptic & physiological saline group( P ＜ 0.05), indicating statistical significance.CONCLUSION: 2-CAdo can reduce apoptosis of hippoeampal neural cells after epilepsy seizure and provide a certain protection for neural cells.
