内科理论与实践

内科理论与实践 ›› 2025, Vol. 20 ›› Issue (06): 457-461.doi: 10.16138/j.1673-6087.2025.06.05

• 论著 • 上一篇    下一篇

紫花前胡素在动脉粥样硬化中的抗炎作用及其药物安全性评估

陈辉1,*(), 杨玲1,*, 赵安琪1, 查晴1, 杨克2, 刘艳1,*()   

  1. 1.上海交通大学医学院附属第九人民医院心血管内科，上海　200011
    2.上海交通大学医学院附属瑞金医院心血管内科，上海　200025
  • 收稿日期:2025-01-03 出版日期:2025-12-30 发布日期:2026-01-30
  • 通讯作者: 刘　艳　E-mail：liuyan0321@sjtu.deu.cn
  • 作者简介:*：陈辉与杨玲为并列第一作者
  • 基金资助:
    国家自然科学基金项目(82070401)

Anti-inflammatory effects and safety evaluation of decursin in atherosclerosis

CHEN Hui1,*(), YANG Ling1,*, ZHAO Anqi1, ZHA Qing1, YANG Ke2, LIU Yan1,*()   

  1. 1. Department of Cardiovascular Medicine, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, China
    2. Department of Cardiovascular Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China
  • Received:2025-01-03 Online:2025-12-30 Published:2026-01-30

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摘要：

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。

关键词: 动脉粥样硬化, 巨噬细胞, 炎症, 核因子κB, 紫花前胡素

Abstract:

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.

Key words: Atherosclerosis, Macrophage, Inflammation, Nuclear factor-κB, Decursin

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