神经科学通报（英文版）
神經科學通報（英文版）
신경과학통보（영문판）
NEUROSCIENCE BULLETIN
2007年
4期
221-228
,共8页
刘颖%陆锦标%陈琦%叶诸榕
劉穎%陸錦標%陳琦%葉諸榕
류영%륙금표%진기%협제용
细胞外信号调节激酶%丝裂原活化蛋白激酶%自由基%碱性成纤维细胞生长因子%早期生长反应因子-1%星形胶质细胞
細胞外信號調節激酶%絲裂原活化蛋白激酶%自由基%堿性成纖維細胞生長因子%早期生長反應因子-1%星形膠質細胞
세포외신호조절격매%사렬원활화단백격매%자유기%감성성섬유세포생장인자%조기생장반응인자-1%성형효질세포
extracellular signal-regulated kinase%mitogen-activated protein kinase%free radicals%fibroblast growth factor 2%early growth response protein 1%astrocyte
目的 静脉注射碱性成纤维细胞生长因子(basic fibroblast growth factor,bFGF)可以明显降低实验性脑缺血大鼠的脑梗死面积,但该作用的分子机制尚不清楚.本文旨在研究外源性bFGF作用的信号转导通路.方法 缺氧-复氧损伤星形胶质细胞.Western blot检测外源性bFGF作用后丝裂原活化蛋白激酶/细胞外信号调节激酶激酶(mitogen-activated protein kinase/extracellular signal-regulated kinase kinase,MEK)-细胞外信号调节激酶(extracellular signal-regulated kinase,ERK)信号通路活化.电泳变动迁移率分析实验检测外源性bFGF作用后核转录因子早期生长反应因子-1(early growth responsfactor 1,Egr-1)的结合活性变化.结果 外源性bFGF可以保护胞外信号调节激酶MEK-ERK信号通路蛋白不被氧自由基降解.MEK-ERK信号通路在外源性bFGF作用后活化.这一信号通路进一步使Egr-1结合活性升高.结论 外源性bFGF可能通过激活ERK信号通路,促进内源性转录因子Egr-1的结合活性升高,进而促进内源性bFGF的表达.
目的 靜脈註射堿性成纖維細胞生長因子(basic fibroblast growth factor,bFGF)可以明顯降低實驗性腦缺血大鼠的腦梗死麵積,但該作用的分子機製尚不清楚.本文旨在研究外源性bFGF作用的信號轉導通路.方法 缺氧-複氧損傷星形膠質細胞.Western blot檢測外源性bFGF作用後絲裂原活化蛋白激酶/細胞外信號調節激酶激酶(mitogen-activated protein kinase/extracellular signal-regulated kinase kinase,MEK)-細胞外信號調節激酶(extracellular signal-regulated kinase,ERK)信號通路活化.電泳變動遷移率分析實驗檢測外源性bFGF作用後覈轉錄因子早期生長反應因子-1(early growth responsfactor 1,Egr-1)的結閤活性變化.結果 外源性bFGF可以保護胞外信號調節激酶MEK-ERK信號通路蛋白不被氧自由基降解.MEK-ERK信號通路在外源性bFGF作用後活化.這一信號通路進一步使Egr-1結閤活性升高.結論 外源性bFGF可能通過激活ERK信號通路,促進內源性轉錄因子Egr-1的結閤活性升高,進而促進內源性bFGF的錶達.
목적 정맥주사감성성섬유세포생장인자(basic fibroblast growth factor,bFGF)가이명현강저실험성뇌결혈대서적뇌경사면적,단해작용적분자궤제상불청초.본문지재연구외원성bFGF작용적신호전도통로.방법 결양-복양손상성형효질세포.Western blot검측외원성bFGF작용후사렬원활화단백격매/세포외신호조절격매격매(mitogen-activated protein kinase/extracellular signal-regulated kinase kinase,MEK)-세포외신호조절격매(extracellular signal-regulated kinase,ERK)신호통로활화.전영변동천이솔분석실험검측외원성bFGF작용후핵전록인자조기생장반응인자-1(early growth responsfactor 1,Egr-1)적결합활성변화.결과 외원성bFGF가이보호포외신호조절격매MEK-ERK신호통로단백불피양자유기강해.MEK-ERK신호통로재외원성bFGF작용후활화.저일신호통로진일보사Egr-1결합활성승고.결론 외원성bFGF가능통과격활ERK신호통로,촉진내원성전록인자Egr-1적결합활성승고,진이촉진내원성bFGF적표체.
Objective Intravenous administration of basic fibroblast growth factor (bFGF) is effective to reduce the volume of cerebral infract due to ischemia. This study was designed to investigate the molecular mechanism, especially the signal transduction pathways, involved in this protective role of bFGF. Methods Anoxia-reoxygenation treated atrocytes were used to study the role of mitogen-activated protein kinase/extracellular signal-regulated kinase kinase (MAPK/ERK kinase, MEK)-ERK signaling pathway after exogenous bFGF administration by Western blot. Electrophoretic mobile shift assay was used to detect the binding activity of early growth response factor-1 (Egr-1), an important transcription factor for endogenous bFGF. Results bFGF could protect some signal transduction proteins from the oxygen-derived free radicals induced degradation. ERK1/2 was activated and involved in Egr-1 binding activity enhancement induced by exogenous bFGF. Conclusion MEK-ERK MAPK cascade may be an important signal transduction pathway contributed to bFGF induced enhancement of Egr- 1 binding activity in anoxia-reoxygenation injured astrocytes.
