摘要
目的 研究肾上腺素对脂多糖 (LPS)诱导的小鼠单核巨噬细胞株RAW 2 6 4 7中肿瘤坏死因子 (TNF α)、一氧化氮 (NO)、环加氧酶 2 (COX 2 )等表达的影响。方法 以 10ng/ml的LPS刺激体外培养的RAW 2 6 4 7细胞作为炎症模型 ,加入不同浓度的肾上腺素 (1× 10 -6,5× 10 -6,1× 10 -5,5× 10 -5mol/L)孵育 2 4h后 ,收集培养上清并提取细胞总蛋白 ,酶联免疫法测定上清中TNF α浓度 ,Griess法检测上清NO含量 ,免疫印迹法检测细胞总蛋白中COX 2的表达量。结果 10ng/ml的LPS明显诱导TNF α、NO、COX 2的产生 ,这一效应可被肾上腺素抑制 ;而单独加入肾上腺素时 ,对上述 3种炎症介质的表达无明显影响。结论 肾上腺素下调LPS诱导的巨噬细胞中炎症因子的表达 ,可能对炎症的发生发展起到一定的调节作用。
Objective To investigate the effects of epinephrine on lipopolysacchride(LPS)-induced pro-inflammatory mediators production such as TNF-α, NO and COX-2 in murine macrophage line RAW264.7. Methods RAW264.7 cells were cultured in vitro with 10 ng/ml LPS in the absence or presence of epinephrine at variant concentrations (1×10 -6, 5×10 -6, 1×10 -5, 5×10 -5 mol/L) for 24 h, then the supernatants were collected for measuring TNF-α by ELISA kit and Griess reagent was used to measure NO concentration respectively. At the same time point, cells were harvested and COX-2 expression was detected by Western blot.Results 10 ng/ml LPS significantly induced the production of TNF-α, NO and COX-2. When epinephrine in combination with LPS was added into the medium, the pro-inflammatory mediators production was suppressed in a dose-dependent manner. However, epinephrine alone had no effect on these inflammatory mediators. Conclusion Epinephrine down-regulates LPS-induced pro-inflammatory mediators production in macrophage, which probably participates in the development of inflammation.
出处
《华中科技大学学报（医学版）》
CAS
CSCD
北大核心
2004年第5期538-540,共3页
Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
基金
国家自然科学基金资助项目 (No . 30 0 70 92 9
No .30 2 0 0 373)
