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山东大学学报 (医学版) ›› 2025, Vol. 63 ›› Issue (9): 77-83.doi: 10.6040/j.issn.1671-7554.0.2025.0019

• 综述 • 上一篇    

基于脂质沉积抑制-代谢清除协同效应的黄连素抗动脉粥样硬化机制研究进展

李习平1,邱梅2,黄瑞峰2,林慧慧2,刘丝丝2,罗鸿莹2,王宇月2,王敏2,杨晓彤3   

  1. 1.贵州中医药大学第一附属医院急诊科, 贵州 贵阳 550001;2.贵州中医药大学基础医学院, 贵州 贵阳 550025;3.贵州中医药大学第一附属医院院办公室, 贵州 贵阳 550001
  • 发布日期:2025-09-08
  • 通讯作者: 王敏. E-mail:2449472505@qq.com杨晓彤. E-mail:tafeng@sina.cn
  • 基金资助:
    贵州省科技厅基础研究计划(自然科学类)科技基金项目(黔科合基础-ZK[2024]一般403)(黔科合基础MS〔2025〕162);贵州省教育厅高等学校自然科学研究项目(青年科技人才成长项目)(黔教技[2024]120号);贵州省卫生健康委科技基金项目(gzwkj2025-347);贵州中医药大学学术新苗项目(贵科合学术新苗[2023]-04号);贵州省科技计划项目(黔科合支撑[2021]一般021);贵州省卫生健康委科技基金项目(gzwkj2025-252);贵州中医药大学护理学院院级项目(HL2406003);贵州中医药大学研究生科研基金项目(YCXKYS2024008)(YCXKYB2023011)

Research progress on the mechanism of berberines anti-atherosclerosis effects based on the synergistic effect of lipid deposition inhibition and metabolic clearance

LI Xiping1, QIU Mei2, HUANG Ruifeng2, LIN Huihui2, LIU Sisi2, LUO Hongying2, WANG Yuyue2, WANG Min2, YANG Xiaotong3   

  1. 1. Department of Emergency, The First Affiliated Hospital of Guizhou University of Traditional Chinese Medicine, Guiyang 550001, Guizhou, China;
    2. School of Basic Medical Sciences, Guizhou University of Traditional Chinese Medicine, Guiyang 550025, Guizhou, China;
    3. Hospital Office, The First Affiliated Hospital of Guizhou University of Traditional Chinese Medicine, Guiyang 550001, Guizhou, China
  • Published:2025-09-08

摘要: 动脉粥样硬化(atherosclerosis, AS)作为心脑血管疾病的主要病理基础,已成为重大公共卫生挑战。现有治疗药物在调控脂质代谢紊乱与炎症反应失衡的协同效应方面存在局限,促使研究者转向具有多靶点调控特性的天然药物。黄连素作为代表性的天然化合物,通过对脂质的“沉积抑制-代谢清除”双重机制发挥抗AS作用。本文论述了黄连素在AS病理进程中调控脂质-炎症网络失衡的作用机制与分子特征,并评述了其临床转化潜力,旨在为突破现有单靶点药物疗效瓶颈提供理论依据和策略指导。

关键词: 黄连素, 动脉粥样硬化, 脂质代谢, 胆固醇, 巨噬细胞

Abstract: Atherosclerosis(AS), the primary pathological basis of cardiovascular diseases, poses a growing global public health challenge. Current therapies face limitations in synergistically addressing lipid metabolism disorders and inflammatory dysregulation, prompting exploration of multi-target natural agents. Berberine, a natural compound, combats AS through dual mechanisms: suppressing cholesterol biosynthesis, enhancing reverse cholesterol transport, and inhibiting macrophage foam cell formation to reduce arterial lipid deposition; while improving lipoprotein homeostasis and activating fatty acid β-oxidation to diminish visceral fat accumulation. These actions collectively prevent AS progression, ameliorate metabolic syndrome, and alleviate hepatic lipotoxicity. This review elucidates berberines molecular mechanisms in rebalancing lipid-inflammatory networks during AS pathogenesis and evaluates its clinical potential, offering novel strategies to overcome single-target drug limitations.

Key words: Berberine, Atherosclerosis, Lipid metabolism, Cholesterol, Macrophages

中图分类号: 

  • R543.1
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