目的：探讨紫花前胡素在动脉粥样硬化疾病中的抗炎作用及其安全性，并验证其对巨噬细胞炎症反应的调节作用。方法：构建高脂饮食喂养的载脂蛋白E基因敲除（apolipoprotein E deficient, ApoE^-/-）雄性小鼠动脉粥样硬化模型，通过氧化型低密度脂蛋白（oxidized low-density lipoprotein, oxLDL）刺激RAW 264.7巨噬细胞以诱导泡沫细胞形成。采用油红O（oil red O, ORO）染色评估主动脉斑块面积减少比例。通过蛋白质印迹检测核因子κB（nuclear factor κB, NF-κB）的磷酸化水平，采用炎症因子阵列分析血清及细胞上清中炎症因子水平，并通过苏木精-伊红（hematoxylin-eosin, HE）染色评估紫花前胡素的全身毒性。结果：紫花前胡素显著减少主动脉斑块面积，在oxLDL刺激的巨噬细胞中，其可抑制NF-κB的过度活化，下调促炎因子[如白介素（interleukin, IL）-2和干扰素（interferon, IFN）-γ]的表达，同时上调抗炎因子（如IL-4和IL-10）的水平。此外，在ApoE^-/-小鼠模型中，紫花前胡素同样显著降低了血清中促炎因子水平，提高抗炎因子水平。HE染色结果显示，紫花前胡素未对主要器官造成明显的病理损伤。结论：紫花前胡素通过调控巨噬细胞炎症反应发挥显著的抗炎作用，并减轻动脉粥样硬化病变，安全性较高，有望成为治疗动脉粥样硬化的潜在药物。

Objective To investigate the anti-inflammatory effects and safety of decursin in atherosclerosis, and to verify its regulatory role in macrophage inflammatory responses. Methods An atherosclerosis model was established using apolipoprotein E deficient (ApoE^-/-) male mice fed a high-fat diet. RAW 264.7 macrophages were stimulated with oxidized low-density lipoprotein (oxLDL) to induce foam cell formation. Oil Red O (ORO) staining was employed to measure the reduction in aortic plaque area. Western blotting was performed to detect the phosphorylation levels of nuclear factor-κB (NF-κB). Inflammatory cytokine levels in serum and cell supernatants were analyzed using inflammatory cytokine arrays. Systemic toxicity of decursin was assessed by hematoxylin-eosin (HE) staining. Results Decursin significantly reduced aortic plaque area and inhibited the excessive activation of NF-κB in oxLDL-stimulated macrophages. It downregulated the expression of pro-inflammatory cytokines [interleukin (IL)-2 and interferon (IFN)-γ] while upregulating anti-inflammatory cytokines (IL-4 and IL-10). Furthermore, in the ApoE^-/- mouse model, decursin similarly significantly lowered serum levels of pro-inflammatory cytokines and elevated those of anti-inflammatory cytokines. HE staining results showed that decursin caused no obvious pathological damage to major organs.Conclusions Decursin exerts significant anti-inflammatory effects by regulating macrophage inflammatory responses, alleviates atherosclerotic lesions, and demonstrates a high safety profile, suggesting its potential as a therapeutic agent for atherosclerosis.