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出 处:《药学学报》1999年第8期586-589,共4页Acta Pharmaceutica Sinica
基 金:国家自然科学基金
摘 要:目的:建立炎性刺激剂诱导细胞核因子κB(NuclearfactorκB,NFκB)的模型,研究传统非甾体抗炎药阿斯匹林(aspirin)作用机理。方法:用脂多糖(LPS)和佛波酯(PMA)刺激小鼠腹腔巨噬细胞,用电泳迁移率改变检测法(electrophoreticmobilityshiftasay,EMSA)检测。结果:LPS1μg·mL-1及3μg·mL-1,PMA2ng·mL-1均能诱导细胞核内NFκB的含量。阿斯匹林10-5mol·L-1可以显著抑制LPS(1μg·mL-1)和PMA(PMA2ng·mL-1)对细胞核内NFκB的活化。结论:所建立的以LPS和PMA为刺激剂,诱导细胞核内NFκB的模型,可用于非甾体抗炎药的抗炎机理的研究。AIM: To establish the model of determining nuclear factor κB(NF κB) which is stimulated by different inflammatory irritants in inducible peritoneal macrophages from mouse and investigate the inhibitory effect of aspirin on NF κB activation using this model. METHODS: Lipopolysaccharide(LPS) and phorbol 12 myristate, 13 acetate(PMA) were used as irritants. Electrophoretic mobility shift assay (EMSA) was used as the determination method. RESULTS: LPS(μg·mL -1 , 3 μg·mL -1 ) and PMA (1 ng·mL -1 ) was shown to increase the content of NF κB in inducible peritoneal macrophages from the mouse. After the macrophages were treated with aspirin(10 -7 mol·L -1 , 10 -6 mol·L -1 , 10 -5 mol·L -1 ), the increase was inhibited. CONCLUSION: The model of determining NF κB stimulated by LPS and PMA can be used in researching mechanism of non steroidal anti inflammatiory drugs.
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