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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 respons factor 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。
The purpose of intravenous injection of basic fibroblast growth factor (bFGF) can significantly reduce cerebral infarction area of experimental cerebral ischemia in rats, but the molecular mechanism of this effect is not clear. This article aims to study the role of exogenous bFGF signal transduction pathway. Methods Hypoxia - reoxygenation injury of astrocytes. Western blot was used to detect the expression of mitogen-activated protein kinase / extracellular signal-regulated kinase kinase (MEK) -expressing extracellular signal-regulated kinase , ERK) signaling pathway activation. The change of binding activity of nuclear transcription factor early growth response factor-1 (Egr-1) after exogenous bFGF treatment was detected by electrophoretic mobility shift assay. Results Exogenous bFGF protected the extracellular signal-regulated kinase MEK-ERK signaling pathway protein from degradation by oxygen free radicals. The MEK-ERK signaling pathway is activated by exogenous bFGF. This signaling pathway further increases Egr-1 binding activity. Conclusion Exogenous bFGF may promote the binding activity of endogenous transcription factor Egr-1 through activation of ERK signaling pathway, thereby promoting the expression of endogenous bFGF.