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一氧化氮调节脂多糖致炎大鼠肺泡巨噬细胞糖皮质激素受体功能的研究

Regulation of nitric oxide on glucocorticoid receptor function in rat alveolar macrophages treated by LPS in vitro
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摘要 目的 研究肺泡巨噬细胞在脂多糖(LPS)作用条件下一氧化氮供体(SNP)对糖皮质激素受体(GR)功能的调节作用。方法 将GR荧光表达质粒pGFP GR转染大鼠肺泡巨噬细胞,经LPS和SNP作用后,荧光显微镜观察质粒表达产物GFP GR核移位情况;相对荧光素酶法检测GR转录激活活性;EMSA检测检测细胞NF κB活性。结果 5 0 0 μmol LSNP作用2h出现GFP GR核移位,同时GR转录激活活性显著增强,NF κB活性被显著抑制。运用GR特异性拮抗剂RU486后,NF κB活性抑制现象消失。结论 肺泡巨噬细胞在致炎因子作用条件下,一氧化氮供体(5 0 0 μmol LSNP )通过活化GR发挥抗炎活性。 Objective To investigate the effects of nitric oxide donor (SNP) on glucocorticoid receptor function in condition of cell inflammation. Methods After fluorescence expression plasmid pGFP-GR transfected rat alveolar macrophges (AMs), nuclear translocation of GFP-GR following to lipopolysaccharide (LPS) and SNP treatment was observed through fluorescence microscope. The transcriptional activation activity of GR was evaluated by the method of relative activity of luciferase. Electrophoretic mobility shift assays (EMSA) were used to measure the activity of NF-κB. Results GFP-GR showed nuclear translocation in 2 h after nitric oxide donor (500 μmol/L SNP) treatment, and the transcriptional activation activity of GR increased and the activity of NF-κB decreased remarkedly. The phenomena of depressed activity of NF-κB disappeared after the addition of GR special antagonism RU486. Conclusion Nitric oxide donor (500 μmol/L SNP) exerts anti-inflammatory effect through GR activation in condition of cell inflammation.
出处 《第三军医大学学报》 CAS CSCD 北大核心 2005年第12期1223-1225,共3页 Journal of Third Military Medical University
基金 国家自然科学基金资助项目 ( 39970 32 9)~~
关键词 一氧化氮供体 糖皮质激素受体 NF-κB 转录激活活性 nitric oxide donor glucocorticoid receptor NF-κB transcriptional activation activity
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