Jiang Shuntao, Gao Kui, Zhang Furong, Wang Yanli, He Xiaojing, Yang Jun
Department of Cardiovascular Medicine, Affiliated Hospital of Zunyi Medical University, No. 149, Dalian Road, Huichuan District, Zunyi, 563000, Guizhou, China.
Department of Cardiology, People's Hospital of Lanshan District, NO.566, Lanshan West Road, Lanshan District, Rizhao, 276800, Shandong, China.
Heliyon. 2024 Aug 2;10(15):e35639. doi: 10.1016/j.heliyon.2024.e35639. eCollection 2024 Aug 15.
The aim of this study is to investigate the main active components of Gegen () on atherosclerosis and its mechanism of action. Bioinformatics analysis showed that β-sitosterol was the most likely active ingredient to mediate the anti-atherosclerotic effects. experiments showed that β-sitosterol inhibited plaque formation and platelet activation, and decreased serum total cholesterol (TC) and triglyceride (TG) levels. experiments showed that β-sitosterol can inhibit lipid deposition and phenotypic transformation of vascular smooth muscle cells (VSMCs). However, knocking down catalase (CAT), the direct target of β-sitosterol, not only promoted lipid deposition and phenotypic transformation of VSMCs, but also activated the PI3K/Akt/mTOR pathway, and the mTOR inhibitor (ink-128) can eliminate the effect of CAT knockdown, suggesting that β-sitosterol may inhibit lipid deposition and phenotypic transformation of VSMCs by activating CAT and silencing the PI3K/Akt/mTOR signaling pathway, thereby alleviating atherosclerosis.
本研究旨在探讨葛根（）抗动脉粥样硬化的主要活性成分及其作用机制。生物信息学分析表明，β-谷甾醇是介导抗动脉粥样硬化作用最可能的活性成分。实验表明，β-谷甾醇可抑制斑块形成和血小板活化，并降低血清总胆固醇（TC）和甘油三酯（TG）水平。实验表明，β-谷甾醇可抑制血管平滑肌细胞（VSMC）的脂质沉积和表型转化。然而，敲低β-谷甾醇的直接靶点过氧化氢酶（CAT），不仅促进了VSMC的脂质沉积和表型转化，还激活了PI3K/Akt/mTOR信号通路，而mTOR抑制剂（INK-128）可消除CAT敲低的作用，提示β-谷甾醇可能通过激活CAT和沉默PI3K/Akt/mTOR信号通路来抑制VSMC的脂质沉积和表型转化，从而减轻动脉粥样硬化。
