中文摘要：

目的探讨肝枯否细胞血管紧张素Ⅱ1型受体（AT-1受体）基因静默对肝枯否细胞NF—κB信号通路的影响。方法采用原代分离培养的肝枯否细胞，免疫组化检测AT-1受体在肝枯否细胞的表达。构建pSilencer／AT—1α受体siRNA质粒，将其转染肝枯否细胞，予10^-4mol／L血管紧张素Ⅱ（AngⅡ）刺激60min，设立阴性对照。凝胶电泳移动抑制实验检测NF—κB DNA结合活性。结果肝枯否细胞可以表达AT-1受体。AngⅡ可刺激肝枯否细胞NF-κB DNA结合活性增强：pSilencer／AT-1α受体siRNA转染细胞后可显著抑制AngⅡ诱导的NF—κB DNA结合活增强。结论AngⅡ可经肝枯否细胞AT-1α受体激活肝枯否细胞NF-κB活性。

英文摘要：

Objective To investigate the effect of angiotensin Ⅱ type-1 （AT-1）α receptor gene silencing on nuclear factor-κB （NF-κB） activity in hepatic Kupffer cells. Methods The expression of AT-1 α receptors in primary isolated cultured hepatic Kupffer cells was detected by immunohistochemistry, pSilencer/AT-1α receptor siRNA plasmids were transfected into Kupffer cells, which were subsequently exposed to 10^-6 mol/L angiotensin Ⅱ （Ang Ⅱ） for 60 min. The changes in the DNA binding activity of NF-κB in the cells was assessed using electrophoretic gel mobility shift assay （EMSA）. Results AT-1α receptor expression was detected in Kupffer cells. NF-κB DNA binding activity was markedly increased in Kupffer cells after Ang Ⅱ stimulation, and obviously inhibited by transfectiom with pSilencer/AT-1α receptor siRNA plasmid. Conclusion Ang Ⅱ stimulation of Kupffer cell results in increased activation of NF-κB via AT-1α receptor.