以千里光石油醚提取物（PEESS）為材料，以脂多糖（LPS）誘導的RAW264.7小鼠單核巨噬細胞為炎癥模型，通過CCK-8法檢測細胞增殖、Griess法檢測一氧化氮（NO）含量、RT-PCR法檢測炎癥相關因子的表達，及Western blot法檢測炎癥關鍵轉錄激活因子的活化，研究PEESS的抗炎作用及可能的分子機制。結果顯示，0~80 μg/mL的PEESS對巨噬細胞增殖無明顯影響，但能顯著抑制LPS誘導的RAW264.7細胞NO的分泌，并呈濃度依賴性；炎癥相關因子基因mRNA表達檢測結果顯示：PEESS能顯著抑制LPS刺激的RAW264.7 細胞炎癥模型中IL-1β及IL-6的表達；同時，PEESS還顯著降低了NF-κB p65及 p44/p22 MAPK蛋白的磷酸化水平。以上結果表明，千里光石油醚提取物對LPS 誘導的RAW264.7 細胞炎癥模型具有較好的抗炎效應，其作用發揮可能與其抑制NF-κB和MAPK信號通路的活化以及NO、IL-1β和IL-6等炎癥介質的分泌有關。
In order to explore the anti-inflammatory effect and its underlying mechanism of Senecio scandens,petroleum ether extract of S. scandens (PEESS) was used to treat the lipopolysaccharide (LPS)-induced RAW264.7 cell. The cell proliferation was detected by CCK-8,the secretion of NO was detected by Griess method,and the expression of inflammation-associated factors was 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 significantly inhibited the secretion of NO in LPS induced RAW264.7 cells by a concentration-dependent manner. Besides,the expression of IL-1β and IL-6 was significantly inhibited by PEESS in LPS induced RAW264.7 cells. Meanwhile,PEESS also significantly reduced the expression of p-NF-κB p65 and p-p44/p22 MAPK proteins. In conclusion,the above results indicated that 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 S. scandens in cuing some inflammatory disease of animals.