基础医学与临床 ›› 2026, Vol. 46 ›› Issue (1): 78-84.doi: 10.16352/j.issn.1001-6325.2026.01.0078

• 研究论文 • 上一篇    下一篇

槲皮素抑制TNF-α诱导的小鼠主动脉血管平滑肌细胞系MOVAS炎性反应

屈改茹1, 席世兵1,2,3, 张宗丽1,2, 李涛1,2,3*   

  1. 十堰市太和医院(湖北医药学院附属医院)1.儿科二病区;
    2.儿童疾病研究所,湖北 十堰 442000;
    3.湖北医药学院 儿童疾病研究所,湖北 十堰 442000
  • 收稿日期:2025-03-14 修回日期:2025-05-27 出版日期:2026-01-05 发布日期:2025-12-29
  • 通讯作者: *317371983@qq.com
  • 基金资助:
    湖北省儿科联盟医学科研项目(HPAMRP202405);十堰市科技局引导性项目(22Y48 24Y040)

Quercetin inhibits TNF-α-induced inflammation of mouse aortic vascular smooth muscle cell line MOVAS

QU Gairu1, XI Shibing1,2,3, ZHANG Zongli1,2, LI Tao1,2,3*   

  1. 1. Department of Pediatrics 2;
    2. Institute of Pediatric Disease, Taihe Hospital, Shiyan 442000;
    3. Institute of Pediatric Disease, Hubei University of Medicine, Shiyan 442000, China
  • Received:2025-03-14 Revised:2025-05-27 Online:2026-01-05 Published:2025-12-29
  • Contact: *317371983@qq.com

摘要: 目的 探究槲皮素(Que)对TNF-α诱导的血管平滑肌细胞(VSMCs)炎性反应的作用及可能的分子机制。方法 将小鼠主动脉血管平滑肌细胞系MOVAS暴露于不同浓度槲皮素中,CCK8法检测槲皮素的细胞毒性;采用TNF-α诱导川崎病(KO)MOVAS细胞炎性反应模型。将其分别暴露于槲皮素和NF-κB p65抑制剂中,用RT-qPCR和Western blot检测炎性因子VCAM-1、ICAM-1、MCP-1、IL-1β、IL-6 及通道蛋白NF-κB p65、磷酸化NF-κB p65的mRNA和蛋白的表达;BCECF-AM荧光探针检测人单核白血病细胞系(THP-1)对MOVAS细胞的黏附能力;免疫荧光法检测NF-κB p65核转位。结果 TNF-α诱导MOVAS细胞炎性反应,即炎性因子VCAM-1、ICAM-1、MCP-1、IL-1β、IL-6的表达(P<0.05)和使THP-1细胞黏附增加(P<0.001);但槲皮素显著降低上述炎性因子的表达以及THP-1细胞黏附(P<0.05)。与对照组相比,槲皮素显著下调TNF-α诱导的MOVAS细胞NF-κB p65亚基的磷酸化(P<0.01)及核转位水平。结论 槲皮素可能通过抑制NF-κB信号通路的激活改善TNF-α诱导的血管平滑肌细胞炎性反应,对川崎病患儿预后可能发挥有益作用。

关键词: 血管平滑肌细胞, 槲皮素, TNF-α, 炎性反应, 川崎病

Abstract: Objective To explore the effect of quercetin(Que)on TNF-α-induced inflammation of vascular smooth muscle cells (VSMCs) and potential mechanism. Methods Mouse aortic vascular smooth cell line MOVAS was exposed to different concentrations of quercetin and the cytotoxicity of quercetin was detected by CCK8 method; TNF-α was used to induce inflammation of MOVAS cells from patients with Kawasaki disease(KO). Cells were exposed to quercetin and NF-κB p65 inhibitors, mRNA and protein expression of inflammatory factors VCAM-1, ICAM-1, MCP-1, IL-1β, IL-6, channel protein NF-κB p65 and phosphorylated NF-κB p65 were detected by RT-qPCR and Western blot; BCECF-AM fluorescent probe was used to detect the adhesion ability of monocytes (THP-1) to MOVAS cells; Immunofluorescence was used to detect NF-κB p65 nuclear translocation. TNF-α significantly induced inflammation of MOVAS cells with expression of inflammatory factors VCAM-1, ICAM-1, MCP-1, IL-1β and IL-6 (P<0.05). THP-1 cells adhesion was significantly increased (P<0.001). However, quercetin significantly reduced the expression of the above inflammatory factors and THP-1 cells adhesion (P<0.05).Quercetin significantly down-regulated phosphorylation (P<0.01) and nuclear translocation levels of NF-κB p65 subunit induced by TNF-α in MOVAS cells as compared to the control group. Conclusions Quercetin potentially plays a beneficial role in Kawasaki disease by inhibiting the activation of the NF-κB signaling pathway to ameliorate TNF-α-induced inflammation of vascular smooth muscle cells.

Key words: vascular smooth muscle cell, quercetin, TNF-α, inflammation, Kawasaki disease

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