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双去甲氧基姜黄素通过促进脂质自噬抑制动脉粥样硬化进展和血管平滑肌细胞源性泡沫细胞形成。

Bisdemethoxycurcumin suppresses the progression of atherosclerosis and VSMC-derived foam cell formation by promoting lipophagy.

作者信息

Zuo Jiangwei, Guo Sien, Qin Xiao

机构信息

Department of Vascular surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, 530021, China.

出版信息

Naunyn Schmiedebergs Arch Pharmacol. 2023 Dec;396(12):3659-3670. doi: 10.1007/s00210-023-02558-7. Epub 2023 Jun 8.

DOI:10.1007/s00210-023-02558-7
PMID:37289282
Abstract

Vascular smooth muscle cells (VSMCs) are one of the sources of foam cells in atherosclerosis. However, the mechanism of VSMC-derived foam cell formation remain largely unknown. Bisdemethoxycurcumin (BDMC) is considered to possess diverse pharmacological properties, including anti-inflammation and anti-oxidation. However, the effects of BDMC on atherosclerosis remain unclear. Here, we established an in vitro foam cell model by culturing VSMCs with oxidized low-density lipoprotein (ox-LDL). The results show that BDMC reduced lipid droplets in ox-LDL-stimulated VSMCs. In addition, BDMC promotes autophagy by suppressing PDK1/Akt/mTOR signaling pathway. In vivo, BDMC alleviates inflammatory responses and lipid accumulation in in apoe mice. Above all, the results from the present study suggested that BDMC may be used as a therapeutic agent for the prevention and treatment of atherosclerosis.

摘要

血管平滑肌细胞(VSMC)是动脉粥样硬化中泡沫细胞的来源之一。然而,VSMC衍生的泡沫细胞形成机制在很大程度上仍不清楚。双去甲氧基姜黄素(BDMC)被认为具有多种药理特性,包括抗炎和抗氧化作用。然而,BDMC对动脉粥样硬化的影响仍不清楚。在此,我们通过用氧化型低密度脂蛋白(ox-LDL)培养VSMC建立了体外泡沫细胞模型。结果表明,BDMC减少了ox-LDL刺激的VSMC中的脂滴。此外,BDMC通过抑制PDK1/Akt/mTOR信号通路促进自噬。在体内,BDMC减轻了载脂蛋白E基因敲除(apoe)小鼠的炎症反应和脂质积累。最重要的是,本研究结果表明BDMC可用作预防和治疗动脉粥样硬化的治疗剂。

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Autophagy. 2021 Sep;17(9):2273-2289. doi: 10.1080/15548627.2020.1822088. Epub 2020 Sep 24.
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