福建医科大学学报
福建醫科大學學報
복건의과대학학보
JOURNAL OF FUJIAN MEDICAL UNIVERSITY
2014年
4期
232-236
,共5页
邵巧燕%戴锦泉%吴斌%施晓容%陈林莺%陈余朋
邵巧燕%戴錦泉%吳斌%施曉容%陳林鶯%陳餘朋
소교연%대금천%오빈%시효용%진림앵%진여붕
奎宁环类%海马%惊厥 ,发热性%脂多糖类%藻酸盐%红藻氨酸%脑损伤%细胞凋亡%疾病模型 ,动物
奎寧環類%海馬%驚厥 ,髮熱性%脂多糖類%藻痠鹽%紅藻氨痠%腦損傷%細胞凋亡%疾病模型 ,動物
규저배류%해마%량궐 ,발열성%지다당류%조산염%홍조안산%뇌손상%세포조망%질병모형 ,동물
Quinuclidines%hippocampus%seizures,febrile%lipopolysaccharides%alginates%kainic acid%brain injuries%apoptosis%disease models,animal
目的:探讨长托宁(盐酸戊乙奎醚注射液)干预对热性惊厥(FS )幼鼠海马神经元损伤的保护作用及其可能机制。方法54只14日龄新生SD幼鼠随机分为3组,即盐水对照组、FS模型组、长托宁干预组,根据处死时间再分为12 h、24 h及48 h亚组。采用低剂量海人藻酸与脂多糖腹腔内注射建立幼鼠FS模型,长托宁干预组在建模同时给予长托宁0.45 mg/kg ,观察比较各组幼鼠惊厥表现,采用苏木精-伊红(H-E)染色法观察记录各组幼鼠海马CA1区神经元结构变化,应用原位末端标记法(TUNEL)观察并记录各组海马神经细胞凋亡数。结果L PS联合低剂量K A诱导FS模型组与长托宁干预组幼鼠惊厥发作,建立FS幼鼠模型。FS模型组、长托宁干预组幼鼠惊厥潜伏期差别无显著性,惊厥持续时间分别为(27.74±6.92)min和(21.74±6.60)min ,惊厥程度评分(级)分别为(3.80±0.94)min和(3.18±0.92)min ,差别均有统计学意义(P均<0.05)。与FS模型组比较,长托宁干预组各时间点海马CA1区神经元变性及丢失程度减轻。与 FS模型组比较,长托宁干预组各时间点海马CA1区TUNEL阳性细胞数均明显减少(P<0.05)。结论长托宁通过减少海马部位神经元细胞凋亡对 FS幼鼠海马神经元有保护作用。
目的:探討長託寧(鹽痠戊乙奎醚註射液)榦預對熱性驚厥(FS )幼鼠海馬神經元損傷的保護作用及其可能機製。方法54隻14日齡新生SD幼鼠隨機分為3組,即鹽水對照組、FS模型組、長託寧榦預組,根據處死時間再分為12 h、24 h及48 h亞組。採用低劑量海人藻痠與脂多糖腹腔內註射建立幼鼠FS模型,長託寧榦預組在建模同時給予長託寧0.45 mg/kg ,觀察比較各組幼鼠驚厥錶現,採用囌木精-伊紅(H-E)染色法觀察記錄各組幼鼠海馬CA1區神經元結構變化,應用原位末耑標記法(TUNEL)觀察併記錄各組海馬神經細胞凋亡數。結果L PS聯閤低劑量K A誘導FS模型組與長託寧榦預組幼鼠驚厥髮作,建立FS幼鼠模型。FS模型組、長託寧榦預組幼鼠驚厥潛伏期差彆無顯著性,驚厥持續時間分彆為(27.74±6.92)min和(21.74±6.60)min ,驚厥程度評分(級)分彆為(3.80±0.94)min和(3.18±0.92)min ,差彆均有統計學意義(P均<0.05)。與FS模型組比較,長託寧榦預組各時間點海馬CA1區神經元變性及丟失程度減輕。與 FS模型組比較,長託寧榦預組各時間點海馬CA1區TUNEL暘性細胞數均明顯減少(P<0.05)。結論長託寧通過減少海馬部位神經元細胞凋亡對 FS幼鼠海馬神經元有保護作用。
목적:탐토장탁저(염산무을규미주사액)간예대열성량궐(FS )유서해마신경원손상적보호작용급기가능궤제。방법54지14일령신생SD유서수궤분위3조,즉염수대조조、FS모형조、장탁저간예조,근거처사시간재분위12 h、24 h급48 h아조。채용저제량해인조산여지다당복강내주사건립유서FS모형,장탁저간예조재건모동시급여장탁저0.45 mg/kg ,관찰비교각조유서량궐표현,채용소목정-이홍(H-E)염색법관찰기록각조유서해마CA1구신경원결구변화,응용원위말단표기법(TUNEL)관찰병기록각조해마신경세포조망수。결과L PS연합저제량K A유도FS모형조여장탁저간예조유서량궐발작,건립FS유서모형。FS모형조、장탁저간예조유서량궐잠복기차별무현저성,량궐지속시간분별위(27.74±6.92)min화(21.74±6.60)min ,량궐정도평분(급)분별위(3.80±0.94)min화(3.18±0.92)min ,차별균유통계학의의(P균<0.05)。여FS모형조비교,장탁저간예조각시간점해마CA1구신경원변성급주실정도감경。여 FS모형조비교,장탁저간예조각시간점해마CA1구TUNEL양성세포수균명현감소(P<0.05)。결론장탁저통과감소해마부위신경원세포조망대 FS유서해마신경원유보호작용。
Objective The main purpose of the present study was to find out whether the penehy-clidine hydrochloride (PHC) has the neuroprotective effect on seizure-induced hippocampal neuron dam-age . Methods Sixty-four cases of 14-day-old Sprague-Dawley rats were divided into three groups ran-domly :the normal saline control group ,the hyperthermic seizure group ,and the PHC treated group . In-traperitoneal injection of LPS combined with KA was used to establish rat model with FS . The rats were injected intraperitoneally with PHC at each time (15 minutes before modeled ,every 12 hour after mod-eled) . Then onset latency ,duration and grade of FS in different groups were observed and compared . Then the histopathology changes in hippocampus were viewed by HE staining and electron-microscope ,the neuron apoptosis was detected by TdT-mediated dUTP nick end labeling (TUNEL) . Results LPS com-bined with KA of intraperitoneal injection can induce febrile seizure . In PHC treated group ,the rats FS duration and FS grade were significantly lower than those in FS control group (P<0 .05) ,although no sig-nificant gap was observed on FS onset latency between them . In FS control group ,HE-staining pattern of hippocampal CA1 region showed lots of disordered neurons with confused polarity and vacuoles formed . <br> While in PHC treated groups ,the arrangement of neurons were regular ,only a small number of neurons had changed . In FS group ,at the 24 h point after seizure ,TUNEL-positive cell in hippocampus CA1 re-gion increased most significantly comparing with PHC treated group (P<0 .05) . Conclusion The pene-hyclidine hydrochloride can lighten the febrile seizure-induced hippocampal neuron damage in rats by inhib-iting cell apoptosis .