论文部分内容阅读
为研究精氨酸双糖苷(AFG)体外的抗炎机制,以脂多糖(LPS)刺激小鼠单核巨噬细胞(RAW264.7)作为炎症模型,用精氨酸双糖苷(AFG)的低、中、高(5、10、20 mg/L)三个剂量进行干预后,MTT法测定细胞毒性作用,Griess法测定一氧化氮(NO)生成量,ELISA法检测细胞上清液中白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)及前列腺素E2(PGE2)的分泌量。结果表明:AFG的三个不同剂量对RAW264.7细胞无抑制作用(P>0.05),各浓度给药组的NO、IL-1β、IL-6、TNF-α和PGE2含量与LPS刺激模型组相比较都显著降低(P<0.01),推想AFG的抗炎活性可能是通过抑制NO和PGE2等炎症介质释放,降低IL-1β、IL-6和TNF-α等炎症因子的含量而发挥了作用。
In order to study the anti-inflammatory mechanism of arginine bisglycoside (AFG) in vitro, monocyte-macrophage cells (RAW264.7) stimulated by lipopolysaccharide (LPS) (5,10 and 20 mg / L), the cytotoxicity was determined by MTT assay, the production of nitric oxide (NO) by Griess assay and the level of interleukin 1β, IL-6, TNF-α and prostaglandin E2 (PGE2) secretion were measured. The results showed that the three different doses of AFG had no effect on RAW264.7 cells (P> 0.05). The concentrations of NO, IL-1β, IL-6, TNF- (P <0.01), suggesting that the anti-inflammatory activity of AFG may play an important role by inhibiting the release of inflammatory mediators such as NO and PGE2 and decreasing the levels of inflammatory factors such as IL-1β, IL-6 and TNF-α .