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<p>Atherosclerosis (AS) remains a leading cause of cardiovascular morbidity worldwide. Strategies that promote autophagy and limit apoptosis hold therapeutic promise. Jingling Granules (JLG), a clinically used formulation, have shown vascular protective effects, but the underlying mechanisms are incompletely understood. Here, we investigated whether JLG attenuates atherosclerosis by modulating autophagy and apoptosis through mTOR signaling. In high-fat diet-fed ApoE<sup>−/−</sup> mice, JLG improved serum lipid profiles, moderately reduced atherosclerotic lesion area, and suppressed systemic inflammation. JLG enhanced autophagic flux and attenuated endothelial cell apoptosis. Mechanistically, JLG downregulated phosphorylated mTOR (p‑mTOR), indicating mTOR pathway inhibition. Consistently, in palmitic acid‑challenged HUVECs, JLG promoted autophagy and reduced apoptosis; these effects were abolished by the mTOR activator MHY1485. Collectively, these findings demonstrate that JLG decelerates atherosclerosis progression by inhibiting mTOR to enhance autophagy and suppress apoptosis, highlighting its therapeutic potential in early stage atherosclerosis.</p>

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Jingling Granules alleviate atherosclerosis through activating autophagy and inhibiting human umbilical vein endothelial cells apoptosis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月29日

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  • Yuhan Wang,
  • Yanzi Liu,
  • Dong Niu,
  • Chang Liu,
  • Qiang Wu,
  • Li Cao,
  • Feng Gao,
  • Shu Lu,
  • Fuming Liu

摘要

Atherosclerosis (AS) remains a leading cause of cardiovascular morbidity worldwide. Strategies that promote autophagy and limit apoptosis hold therapeutic promise. Jingling Granules (JLG), a clinically used formulation, have shown vascular protective effects, but the underlying mechanisms are incompletely understood. Here, we investigated whether JLG attenuates atherosclerosis by modulating autophagy and apoptosis through mTOR signaling. In high-fat diet-fed ApoE−/− mice, JLG improved serum lipid profiles, moderately reduced atherosclerotic lesion area, and suppressed systemic inflammation. JLG enhanced autophagic flux and attenuated endothelial cell apoptosis. Mechanistically, JLG downregulated phosphorylated mTOR (p‑mTOR), indicating mTOR pathway inhibition. Consistently, in palmitic acid‑challenged HUVECs, JLG promoted autophagy and reduced apoptosis; these effects were abolished by the mTOR activator MHY1485. Collectively, these findings demonstrate that JLG decelerates atherosclerosis progression by inhibiting mTOR to enhance autophagy and suppress apoptosis, highlighting its therapeutic potential in early stage atherosclerosis.