为探讨千里光抗炎作用及机制,以千里光石油醚提取物(PEESS)为材料,以脂多糖(LPS)诱导的RAW264.7小鼠单核巨噬细胞为炎症模型,通过CCK-8法检测细胞增殖、Griess法检测NO含量、RT-PCR法及Western blot法检测炎症相关因子表达,研究了PEESS的抗炎作用及可能的分子机制。结果显示,0~80 μg/mL的PEESS对巨噬细胞增殖无明显影响,但能显著抑制LPS诱导的RAW264.7细胞NO的分泌,并呈浓度依赖性；对炎症相关因子基因mRNA表达检测结果表明PEESS能显著抑制LPS 致RAW264.7 细胞炎症模型中IL-1β及IL-6的表达；同时,PEESS还显著降低了p-NF-κB p65及 p-p44/p22 MAPK蛋白的表达。综上,千里光石油醚提取物对LPS 诱导的RAW264.7 细胞炎症模型具有较好抗炎效应,其作用发挥可能与其抑制NO、IL-1β和IL-6等炎症介质的分泌及NF-κB 信号通路和MAPK信号通路的活化有关,为将千里光应用于动物抗炎及探究其具体作用机制奠定了基础。
in order to explore the anti-inflammatory effect and underlying mechanism of Senecio scandens, Petroleum ether extract of Senecio scandens(PEESS)was used to treat the lipopolysaccharide(LPS)-induced inflammation response in mouse mononuclear macrophages RAW264.7. The cell proliferation were detected by CCK-8, and the secretion of NO were detected by Griess method, and the expression of inflammation-associated factors were detected by RT-PCR and Western blot. The results showed that PEESS at 0~80 μg/mL had no significant effect on the proliferation of RAW264.7. However, it can significantly inhibit the secretion of NO in LPS induced RAW264.7 cells by a concentration-dependent manner. And the expression of IL-1β and IL-6 were significantly inhibited by PEESS in LPS induced RAW264.7 cells. Meanwhile, PEESS also significantly reduced the level of p-NF-κB p65 and p-p44/p22 MAPK proteins. In conclusion, PEESS may participate in the process of anti-inflammatory response by inhibiting the expression of some pro-inflammatory mediators such as NO, IL-1β and IL-6, and the activation of the NF-κB and MAPK signaling pathways. This study lays a foundation for the application of Senecio scandens in cuing some inflammatory disease of animals.