中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2012年
7期
1352-1354
,共3页
吴俊%陈旭%舒凯%肖铮铮%雷霆%李龄
吳俊%陳旭%舒凱%肖錚錚%雷霆%李齡
오준%진욱%서개%초쟁쟁%뢰정%리령
颞叶癫痫%海马硬化%c-Jun氨基末端激酶%SP600125
顳葉癲癇%海馬硬化%c-Jun氨基末耑激酶%SP600125
섭협전간%해마경화%c-Jun안기말단격매%SP600125
Temporal lobe epilepsy%Hippocampal sclerosis%C-Jun N-terminal kinase%SP600125
目的 通过对杏仁核电刺激癫痫模型大鼠脑室内注射c-Jun氨基末端激酶(JNK)特异性抑制剂SP600125,观察海马区的病理变化和JNK水平的变化,探讨SP600125的作用.方法 将40只Wistar大鼠随机分为4组:空白组、点燃组、加药组和加药对照组各10只,10次癫痫发作后灌注取脑,Western blot法检测JNK的表达变化,进行尼氏和胶原纤维酸性蛋白(GFAP)染色,各组间进行比较.结果 Western blot显示点燃组海马区的JNK磷酸化水平(0.48±0.04)较空白组(0.38±0.04)和加药组(0.37±0.03)显著增高(P<0.05),总JNK水平各组之间差异无统计学意义(P>0.05).尼氏染色阳性细胞计数加药组(33.41±3.73)较加药对照组(20.10±5.11)显著增高(P<0.05).点燃组GFAP阳性细胞计数(65.45±4.53)和加药对照组(67.18±3.52)较空白组(40.37±3.82)和加药组(43.51±1.83)显著增加(P<0.05).结论 JNK信号通路可能参与颞叶癫痫海马硬化形成,表现为磷酸化JNK升高,SP600125通过抑制JNK可以缓解海马区病理变化.
目的 通過對杏仁覈電刺激癲癇模型大鼠腦室內註射c-Jun氨基末耑激酶(JNK)特異性抑製劑SP600125,觀察海馬區的病理變化和JNK水平的變化,探討SP600125的作用.方法 將40隻Wistar大鼠隨機分為4組:空白組、點燃組、加藥組和加藥對照組各10隻,10次癲癇髮作後灌註取腦,Western blot法檢測JNK的錶達變化,進行尼氏和膠原纖維痠性蛋白(GFAP)染色,各組間進行比較.結果 Western blot顯示點燃組海馬區的JNK燐痠化水平(0.48±0.04)較空白組(0.38±0.04)和加藥組(0.37±0.03)顯著增高(P<0.05),總JNK水平各組之間差異無統計學意義(P>0.05).尼氏染色暘性細胞計數加藥組(33.41±3.73)較加藥對照組(20.10±5.11)顯著增高(P<0.05).點燃組GFAP暘性細胞計數(65.45±4.53)和加藥對照組(67.18±3.52)較空白組(40.37±3.82)和加藥組(43.51±1.83)顯著增加(P<0.05).結論 JNK信號通路可能參與顳葉癲癇海馬硬化形成,錶現為燐痠化JNK升高,SP600125通過抑製JNK可以緩解海馬區病理變化.
목적 통과대행인핵전자격전간모형대서뇌실내주사c-Jun안기말단격매(JNK)특이성억제제SP600125,관찰해마구적병리변화화JNK수평적변화,탐토SP600125적작용.방법 장40지Wistar대서수궤분위4조:공백조、점연조、가약조화가약대조조각10지,10차전간발작후관주취뇌,Western blot법검측JNK적표체변화,진행니씨화효원섬유산성단백(GFAP)염색,각조간진행비교.결과 Western blot현시점연조해마구적JNK린산화수평(0.48±0.04)교공백조(0.38±0.04)화가약조(0.37±0.03)현저증고(P<0.05),총JNK수평각조지간차이무통계학의의(P>0.05).니씨염색양성세포계수가약조(33.41±3.73)교가약대조조(20.10±5.11)현저증고(P<0.05).점연조GFAP양성세포계수(65.45±4.53)화가약대조조(67.18±3.52)교공백조(40.37±3.82)화가약조(43.51±1.83)현저증가(P<0.05).결론 JNK신호통로가능삼여섭협전간해마경화형성,표현위린산화JNK승고,SP600125통과억제JNK가이완해해마구병리변화.
Objective By injecting SP600125 into ventricle of amygdale kindled rats,to observe the pathological changes of the hippocampus and the change of C-Jun N-terminal kinase (JNK) phosphorylation,and discuss the action mechanism of SP600125.Methods Forty rats were randomly divided into 4 groups (n =10 each):blank group,kindling group,SP600125 group,DMSO group.Whole-cell extracts of tissues were obtained from the right hippocampus,and Western blotting was used to detect the changes of JNK and phosphorylation of JNK.Pathological changes of the hippocampus and amygdla were observed by GFAP stain and Nissl stain.Results The level of JNK phosphorylation in the hippocampus was significantly higher in the kindling group (0.48 ± 0.04 ) than the blank group (0.38 ± 0.04 ) and the SP600125 group (0.37±0.03).Nissl stain positive cells in the hippocampus of the SP600125 group were significantly more than those in the the DMSO group (20.10 ±5.11 ).The expression of GFAP in the hippocampus of kindling group (65.45 ±4.53 ) and DMSO group (67.18 ± 3.52) was significantly stronger than that in the blank group (40.37 ± 3.82) and the SP600125 group (43.51 ± 1.83).Conclusion The role of repeated activation of JNK can be related to the hippocampal sclerosis in these rats.SP600125 had a protective effect on neurons during the kindling procedure.