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<p>Coronary heart disease (CHD) is a disease caused by organic and functional coronary artery stenosis, resulting in a reduced oxygen supply to the heart. This study aimed to investigate the mechanism via which Luteolin regulates the <i>Sirt1</i>/<i>Nrf2</i> pathway to inhibit ferroptosis in human umbilical vein endothelial cells (HUVEC) associated with CHD. An ox-LDL-induced HUVEC cell model with <i>Sirt1</i> silencing and Luteolin treatment was established. The silencing efficiency of <i>Sirt1</i> was validated using quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blot analysis. The results of molecular docking and DARTS experiments showed that Luteolin could effectively bind <i>Sirt1</i>. Subsequently, we measured the expression of <i>Nrf2</i> and <i>Sirt1</i>, cell viability, MDA, GSH, Fe<sup>2+</sup> levels, lipid ROS content, expression of ferroptosis-related proteins GPX4, FTH, FTL, and cell migration parameters. The results showed that Luteolin could activate the <i>Sirt1</i>/<i>Nrf2</i> axis and effectively inhibit ox-LDL-induced ferroptosis in HUVEC. Experimental results revealed that Luteolin could enhance HUVEC cell viability, decrease MDA, Fe<sup>2+</sup>, and ROS levels, increase GSH levels, promote the expression of HO-1, GPX4, FTH, FTL, inhibit the expression of ACSL4 and TFRC, and enhance the migration capability of HUVEC cells. Moreover, silencing <i>Sirt1</i> reversed the effects of Luteolin on the activation of <i>Sirt1</i> and <i>Nrf2</i>, confirming the dependence of these effects on the <i>Sirt1</i>/<i>Nrf2</i> signaling pathway. In conclusion, this study indicates that Luteolin could inhibit ferroptosis in HUVEC in CHD by modulating the <i>Sirt1</i>/<i>Nrf2</i> axis, providing a basis for further research on strategies for preventing and treating CHD and related diseases.</p>

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Luteolin Inhibits Ferroptosis of HUVEC by Regulating the Sirt1/Nrf2 Pathway

  • 期刊论文

  • 发表日期：

    2025年7月28日

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  • Ming Xiang,
  • Xiangdong Lin,
  • Haiying Chen

摘要

Coronary heart disease (CHD) is a disease caused by organic and functional coronary artery stenosis, resulting in a reduced oxygen supply to the heart. This study aimed to investigate the mechanism via which Luteolin regulates the Sirt1/Nrf2 pathway to inhibit ferroptosis in human umbilical vein endothelial cells (HUVEC) associated with CHD. An ox-LDL-induced HUVEC cell model with Sirt1 silencing and Luteolin treatment was established. The silencing efficiency of Sirt1 was validated using quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blot analysis. The results of molecular docking and DARTS experiments showed that Luteolin could effectively bind Sirt1. Subsequently, we measured the expression of Nrf2 and Sirt1, cell viability, MDA, GSH, Fe2+ levels, lipid ROS content, expression of ferroptosis-related proteins GPX4, FTH, FTL, and cell migration parameters. The results showed that Luteolin could activate the Sirt1/Nrf2 axis and effectively inhibit ox-LDL-induced ferroptosis in HUVEC. Experimental results revealed that Luteolin could enhance HUVEC cell viability, decrease MDA, Fe2+, and ROS levels, increase GSH levels, promote the expression of HO-1, GPX4, FTH, FTL, inhibit the expression of ACSL4 and TFRC, and enhance the migration capability of HUVEC cells. Moreover, silencing Sirt1 reversed the effects of Luteolin on the activation of Sirt1 and Nrf2, confirming the dependence of these effects on the Sirt1/Nrf2 signaling pathway. In conclusion, this study indicates that Luteolin could inhibit ferroptosis in HUVEC in CHD by modulating the Sirt1/Nrf2 axis, providing a basis for further research on strategies for preventing and treating CHD and related diseases.