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目的 探讨外源性锌指蛋白A2 0对内毒素 (LPS)诱导的内皮细胞同型半胱氨酸蛋白酶caspase 3表达和凋亡的影响。 方法 RT PCR检测A2 0基因在内毒素诱导内皮细胞中的表达。DOTAP脂质体转染pCDNA3 1EHA2 0于脐静脉内皮细胞 ,经G4 18筛选 ,A2 0表达经免疫荧光鉴定。Tunnel原位末端标记法、原位杂交检测转染前后内毒素诱导内皮细胞凋亡情况及caspase 3的表达情况。 结果 A2 0基因在内毒素诱导的内皮细胞中能表达。正常对照组及转染A2 0基因组人脐静脉内皮细胞 (HUVEC)凋亡为 (5± 1) %、(6± 1) % ,LPS作用后对照组与转染A2 0基因组凋亡分别为 (36± 3) %、(10± 1) % ,两者相差显著 (P <0 0 5 )。A2 0基因能显著抑制内毒素诱导的内皮细胞caspase 3的表达。 结论 A2 0基因在创伤的治疗中可能有一定作用。
Objective To investigate the effect of exogenous zinc finger protein A2 0 on endoplasmic reticulum cysteine proteinase caspase 3 (LPS) -induced apoptosis. Methods RT-PCR was used to detect A2 0 gene expression in endotoxin-induced endothelial cells. DOTAP liposome transfected pCDNA3 1EHA2 0 in umbilical vein endothelial cells, screened by G4 18, A2 0 expression was identified by immunofluorescence. TUNEL staining and in situ hybridization were performed to detect endotoxin-induced endothelial cell apoptosis and caspase 3 expression before and after transfection. Results A2 0 gene can be expressed in endotoxin-induced endothelial cells. Apoptosis of normal control group and A2 0 gene transfected human umbilical vein endothelial cells (HUVEC) were (5 ± 1)% and (6 ± 1)%, respectively. The apoptotic rates of control group and A2 0 gene group after LPS treatment were 36 ± 3)% and (10 ± 1)%, respectively (P <0 05). A2 0 gene can significantly inhibit endotoxin-induced endothelial cell caspase 3 expression. Conclusion A2 0 gene may play a role in the treatment of trauma.