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【目的】探讨外源性锌指蛋白基因A20对缺氧诱导内皮细胞黏附分子CD54表达的影响。【方法】培养原代人脐静脉内皮细胞,将细胞分组建立缺氧模型;采用DOTAP脂质体介导pcDNA3.1EHA20质粒转染培养的内皮细胞,筛选抗G418的阳性克隆,经免疫荧光鉴定A20基因的表达;采用免疫组化和原位杂交检测内皮细胞CD54的表达。【结果】A20基因在经G418筛选后的内皮细胞中得到高效表达。缺氧能诱导人内皮细胞CD54高表达,外源性A20基因能抑制75%以上由缺氧诱导的内皮细胞CD54表达,两者间相差明显(P<0.01)。【结论】外源性A20基因能够显著抑制缺氧诱导的内皮细胞活化,有效抑制CD54的表达,可能在内皮细胞缺氧损伤中具有保护作用。
【Aim】 To investigate the effect of exogenous zinc finger protein gene A20 on hypoxia-induced endothelial cell adhesion molecule CD54 expression. 【Methods】 Primary cultured human umbilical vein endothelial cells (HUVECs) were cultured in vitro and hypoxia cells were divided into groups. DOTAP-mediated plasmid pcDNA3.1EHA20 was used to transfect cultured endothelial cells and positive clones against G418 were screened. A20 The expression of CD54 was detected by immunohistochemistry and in situ hybridization. 【Results】 A20 gene was highly expressed in endothelial cells after G418 selection. Hypoxia can induce high expression of CD54 in human endothelial cells, and exogenous A20 gene can inhibit more than 75% of CD54 expression induced by hypoxia in endothelial cells, with a significant difference between them (P <0.01). 【Conclusion】 Exogenous A20 gene can significantly inhibit the hypoxia-induced endothelial cell activation and effectively inhibit the expression of CD54, which may have a protective effect on endothelial cell injury induced by hypoxia.