福建医科大学学报
福建醫科大學學報
복건의과대학학보
JOURNAL OF FUJIAN MEDICAL UNIVERSITY
2014年
3期
147-150
,共4页
陈琅%陈巧彬%方琼%娄五斌%高学杰%周俊香
陳瑯%陳巧彬%方瓊%婁五斌%高學傑%週俊香
진랑%진교빈%방경%루오빈%고학걸%주준향
癫痫%戊四氮%脑%磷酸丙酮酸水合酶%S100蛋白质类%髓磷脂碱性蛋白质类%大鼠,Sprague-Dawley
癲癇%戊四氮%腦%燐痠丙酮痠水閤酶%S100蛋白質類%髓燐脂堿性蛋白質類%大鼠,Sprague-Dawley
전간%무사담%뇌%린산병동산수합매%S100단백질류%수린지감성단백질류%대서,Sprague-Dawley
epilepsy%pentylenetetrazole%brain%phosphopyruvate hydratase%S100 proteins%my-elin basic proteins%rats,Sprague-Dawley
目的：研究S100B蛋白、碱性髓鞘蛋白（MBP）和神经元特异性烯醇酶（NSE）在戊四氮（PTZ）诱导致痫幼鼠海马、额叶、中脑和血清中的动态改变，评鉴癫痫（EP）造成不同脑区的神经损伤。方法雄性SD幼鼠60只，随机分对照组（10只）和实验组（50只）。实验组腹腔注射（IP）PTZ 50 mg/kg 1次，A组IP生理盐水。根据EP发作分级，0～1级9只视为B组，立即取脑；2级以上发作41只，于EP发作后0 h（C＝10）、6 h（D＝11）、24 h （E＝10）、72 h（F＝10）断头，分别取下海马、中脑和额叶皮质，断头前抽取躯干血。采用ELISA法检测血清和各脑区S100B和MBP ，采用EIA法检测血清和各脑区 NSE值。结果 EP发作后，海马、额叶和血清S100B蛋白、MBP和NSE均明显高于对照组。海马和额叶的NSE峰值出现在中脑NSE之前。各脑区和血清S100B蛋白皆于EP后24 h达高峰，而MBP于EP后72 h达高峰。结论 EP发作可以造成大脑不同脑区神经元细胞、胶质细胞和神经髓鞘的损伤。
目的：研究S100B蛋白、堿性髓鞘蛋白（MBP）和神經元特異性烯醇酶（NSE）在戊四氮（PTZ）誘導緻癇幼鼠海馬、額葉、中腦和血清中的動態改變，評鑒癲癇（EP）造成不同腦區的神經損傷。方法雄性SD幼鼠60隻，隨機分對照組（10隻）和實驗組（50隻）。實驗組腹腔註射（IP）PTZ 50 mg/kg 1次，A組IP生理鹽水。根據EP髮作分級，0～1級9隻視為B組，立即取腦；2級以上髮作41隻，于EP髮作後0 h（C＝10）、6 h（D＝11）、24 h （E＝10）、72 h（F＝10）斷頭，分彆取下海馬、中腦和額葉皮質，斷頭前抽取軀榦血。採用ELISA法檢測血清和各腦區S100B和MBP ，採用EIA法檢測血清和各腦區 NSE值。結果 EP髮作後，海馬、額葉和血清S100B蛋白、MBP和NSE均明顯高于對照組。海馬和額葉的NSE峰值齣現在中腦NSE之前。各腦區和血清S100B蛋白皆于EP後24 h達高峰，而MBP于EP後72 h達高峰。結論 EP髮作可以造成大腦不同腦區神經元細胞、膠質細胞和神經髓鞘的損傷。
목적：연구S100B단백、감성수초단백（MBP）화신경원특이성희순매（NSE）재무사담（PTZ）유도치간유서해마、액협、중뇌화혈청중적동태개변，평감전간（EP）조성불동뇌구적신경손상。방법웅성SD유서60지，수궤분대조조（10지）화실험조（50지）。실험조복강주사（IP）PTZ 50 mg/kg 1차，A조IP생리염수。근거EP발작분급，0～1급9지시위B조，립즉취뇌；2급이상발작41지，우EP발작후0 h（C＝10）、6 h（D＝11）、24 h （E＝10）、72 h（F＝10）단두，분별취하해마、중뇌화액협피질，단두전추취구간혈。채용ELISA법검측혈청화각뇌구S100B화MBP ，채용EIA법검측혈청화각뇌구 NSE치。결과 EP발작후，해마、액협화혈청S100B단백、MBP화NSE균명현고우대조조。해마화액협적NSE봉치출현재중뇌NSE지전。각뇌구화혈청S100B단백개우EP후24 h체고봉，이MBP우EP후72 h체고봉。결론 EP발작가이조성대뇌불동뇌구신경원세포、효질세포화신경수초적손상。
Objective By ELISA and EIA evaluated the levels of S100B protein ,myelin basic pro-tein (MBP) and Neuron-specific enolase (NSE) in the serum ,hippocampus ,mesencephalon and frontal cortex in pentylenetetrazol (PTZ) induced epilepsy young rats to study the brain damage after seizure at-tacked . Methods 60 male aged 4~5 weeks young SD rats were divided into control and experimental groups randomly . The control group(A=10) was injected intraperioneally (IP) with the same value of normal saline and the experimental group was IP with PTZ (50 mg/kg) . The experimental group was di-vided into groups with or without seizure again (B= 9) ,group B was sacrificed immediately . Seizure groups were decapitated at 0 h(C= 10) ,6 h(D= 11) ,24 h(E= 10) and 72 h(F= 10) after seizures . Blood samples were collected before scarify . Enzyme-immunoassay(EIA) was used to evaluate the chan-ges of NSE in mesencephalon ,hippocampus ,frontal cortex and serum . And the ELISA was applied to e-valuate the levels of S100B and MBP . Results The levels of S100B ,MBP and NSE in the seizure groups were significant higher than that of control group . The level of NSE in frontal cortex ,striatum and hip-pocampus of the seizure group was increased after seizure ,and the level of NSE in serum and mesencepha-lon got its highest at 6 hours after seizure ,and then decreased . At 24 hours after seizure ,the level of NSE in the hippocampus and serum was still higher then that of the control group (P<0 .01) . Levels of S100B protein and MBP in serum ,hippocampus ,frontal lobe and mesencephalon were remarkable changes after seizure . Values of S100B protein in different brains and serum got the highest at 24 h after seizure and levels of MBP reached the highest at 72 h after seizure . Conclusion The significant increased levels of S100B protein ,MBP and NSE in the brains and serum of PTZ-induced epilepsy young rats may suggest the damage of neuron cell ,myelin fabric and glial cell .
