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观察持续性局灶性脑缺血 (permanentmiddlecerebralarteryocclusion ,pMCAO)损伤后表达碱性成纤维细胞生长因子 (basicfibroblastgrowthfactor,bFGF)的细胞种类、时相与不同细胞之间的相互影响 ,并探讨Egr 1基因蛋白对bFGF表达的影响。结果表明 :在持续性局灶性脑缺血后 ,缺血梗死灶周边区免疫组化结果显示bFGF表达出现双相增强。缺血 1h缺血边缘区主要在星形胶质细胞 (Astrocyte,As)中bFGF出现一过性增强 ,并见细胞外基质中出现bFGF点状着色。缺血 6h～ 1d时bFGF染色再次增强 ,神经元及各类胶质细胞中的表达均有增强。但是经Western blot定量测定发现脑组织bFGF含量仅在缺血后 6h～ 1d时出现增强。缺血 1h时 ,bFGF可能经缺血细胞受损的细胞膜到达细胞外 ,与细胞外硫酸肝素或相关分子结合 ,内化进入缺血边缘区细胞 ,从而造成bFGF免疫组化染色一过性增强。第二次增强可能是缺血损伤刺激及内化的bFGF诱导的蛋白合成的增加。缺血 2～ 6hbFGFR在神经元及各类胶质细胞中的表达均增强 ,主要位于缺血区的边缘。由于bFGFR表达时程早于bFGF转录合成增加 ,因此限制了内源性bFGF发挥保护缺血损伤神经元的作用 ,这使得外源应用bFGF成为必要。Egr 1基因蛋白的表达在缺血损伤后 1～ 6h增强 ,其表达增高的时相早于bFGF?
To observe the cell types, the interaction between different phases of cells and the expression of basic fibroblast growth factor (bFGF) after permanent focal cerebral ischemia (pMCAO) injury, and to explore the role of Egr 1 gene protein On bFGF expression. The results showed that the immunohistochemical results in peripheral zone of ischemic infarct showed bFGF increased after persistent focal cerebral ischemia. In ischemia 1h ischemic region, bFGF mainly appeared as a transient enhancement in astrocyte (As), and bFGF punctate staining appeared in extracellular matrix. After 6h ~ 1d ischemia, the bFGF staining increased again, the expression of neurons and glial cells increased. However, by Western blot quantitative determination of bFGF content in brain tissue only after 6h ~ 1d after ischemia increased. At 1 hour after ischemia, bFGF may reach the extracellular matrix through the damaged cell membrane of ischemic cells, bind to extracellular heparin sulfate or related molecules, and internalize into the ischemic marginal zone cells, resulting in transient enhancement of bFGF immunohistochemical staining. The second enhancement may be an increase in bFGF-induced protein synthesis that is stimulated by ischemic insult and internalized. Ischemia 2 ~ 6hbFGFR expression in neurons and glial cells were enhanced, mainly located in the edge of the ischemic area. Since bFGFR expression is increased earlier than bFGF transcript synthesis, the role of endogenous bFGF in protecting ischemic neurons is limited, necessitating the exogenous application of bFGF. The expression of Egr 1 protein increased 1 ~ 6 h after ischemic injury, and its expression increased earlier than that of bFGF.