摘要: |
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。 |
关键词: 精氨酸双糖苷 小鼠RAW264.7细胞 抗炎活性 炎症因子 |
DOI: |
投稿时间:2016-08-31修订日期:2016-11-02 |
基金项目:科技型中小企业创新创业基金项目(20160308002YY) |
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Effects of Arginyl-Fructosyl-Glucose on the Secretion of Inflammatory Cytokines in Macrophages Induced by Lipopolysaccharide |
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(Jilin Agricultural University,College of Chinese Medicinal Materials;China) |
Abstract: |
In this paper, we studied the anti-inflammatory mechanism of arginyl-fructosyl-glucose (AFG) in vitro. The inflammation model, which was established based on the mouse monocyte-macrophage cells (RAW264.7) stimulated by lipopolysaccharide (LPS), is intervened by three doses of AFG, low, medium and high (5, 10, 20 mg/L). After intervention, MTT approach was used to access cytotoxicity; Griess approach is used to determine the amount of nitric oxide(NO); and ELISA was used to evaluate the secretion of interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and prostaglandin E2 (PGE2) in cell supernatants. The results that: The three doses of AFG have no inhibition effect on RAW264.7 cells (P>0.05). In the control group, all contents of NO, IL-1β, IL-6, TNF-α and PGE2 are significant less than placebo group (LPS model) (P<0.01). The mechanism of AFG in anti-inflammatory activity may be contributed by inhibiting the release of inflammatory mediators of NO and PGE2, reducing the amount of IL-1β, IL-6, TNF-α and other inflammatory factors. |
Key words: arginyl-fructosyl-glucose(AFG) mouse RAW264.7 cells anti-inflam- matory activity inflammatory factors. |