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<p>Endothelial dysfunction is a critical initiating event in atherosclerosis. Endothelial nitric oxide synthase (eNOS) plays a key role in maintaining vascular health by producing nitric oxide (NO) to regulate vascular tone. Tetrahydrocurcumin (THCu), a stable metabolite of curcumin, exhibits promising bioactivity; however, its precise vasoprotective mechanism remains unclear. This study investigated the hypothesis that THCu enhances eNOS function in human umbilical vein endothelial cells by activating the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway. Our results demonstrate that THCu treatment robustly and dose-dependently increased PI3K and AKT phosphorylation. This upstream activation directly led to eNOS phosphorylation at Ser1177, significantly boosting NO bioavailability. Pharmacological inhibition of PI3K or AKT completely abolished THCu-induced eNOS phosphorylation and NO release. In conclusion, this research delineates a clear mechanistic framework establishing the PI3K/AKT cascade as the essential pathway for THCu-mediated eNOS activation, providing a strong scientific rationale for its further investigation as a candidate for mitigating endothelial dysfunction in atherosclerosis.</p>

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Elucidating the vasoprotective mechanism of Tetrahydrocurcumin: from unbiased transcriptomic discovery to targeted validation of the PI3K/AKT pathway

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年4月10日

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  • Yi-Lin Chiu,
  • Tsai-Jung Lin,
  • Hsing-Fan Lai,
  • Yu-Sin Chang,
  • Tzu-Chiao Lin,
  • Yen-Lien Chou,
  • Cheng-Chung Cheng,
  • Sharon Fong,
  • Tsung-Neng Tsai

摘要

Endothelial dysfunction is a critical initiating event in atherosclerosis. Endothelial nitric oxide synthase (eNOS) plays a key role in maintaining vascular health by producing nitric oxide (NO) to regulate vascular tone. Tetrahydrocurcumin (THCu), a stable metabolite of curcumin, exhibits promising bioactivity; however, its precise vasoprotective mechanism remains unclear. This study investigated the hypothesis that THCu enhances eNOS function in human umbilical vein endothelial cells by activating the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway. Our results demonstrate that THCu treatment robustly and dose-dependently increased PI3K and AKT phosphorylation. This upstream activation directly led to eNOS phosphorylation at Ser1177, significantly boosting NO bioavailability. Pharmacological inhibition of PI3K or AKT completely abolished THCu-induced eNOS phosphorylation and NO release. In conclusion, this research delineates a clear mechanistic framework establishing the PI3K/AKT cascade as the essential pathway for THCu-mediated eNOS activation, providing a strong scientific rationale for its further investigation as a candidate for mitigating endothelial dysfunction in atherosclerosis.