SAL protects endothelial cells from H2O2-induced endothelial dysfunction: Regulation of inflammation and autophagy by EZH2

作者：Sun Li, Xuefang Li, Jie Zhang, Jiachao Pei, Jianhua Zhang, Yinghua Wang, Fei Lin, Guoan Zhao · 发表于：International Immunopharmacology · 年份：2024 · DOI：10.1016/j.intimp.2024.113060 · 被引用次数：6 · 研究领域：Autophagy in Disease and Therapy、Eicosanoids and Hypertension Pharmacology、Hydrogen's biological and therapeutic effects

• SAL improves H 2 O 2 -induced endothelial dysfunction. • EZH2 knockdown enhances the protective effects of SAL on endothelial function. • SAL mitigates H 2 O 2 -induced endothelial dysfunction by modulating EZH2-mediated pathways. • Inhibition of EZH2 by SAL presents a novel therapeutic strategy for inflammation-related vascular diseases. One component of the polycomb repressor complex 2 is histone methyltransferase zeste homolog 2 (EZH2), which is also called Enhancer of zeste homolog 2. It is considered a potential therapeutic target for inhibiting endothelial dysfunction.. Hence, directing efforts towards EZH2 to weaken endothelium damage and regulate vascular lesions proves to be a highly successful therapeutic approach for enhancing endothelial dysfunction. This study aimed to investigate the mechanism by which salidroside (SAL) improves hydrogen peroxide (H 2 O 2 )-induced endothelial dysfunction. The investigation involved the use of many techniques, including western blotting, real-time polymerase chain reaction (RT-PCR), a scratch test, molecular docking, and other methods. The experimental findings demonstrated that SAL has the ability to inhibit the impaired functioning of endothelial cells caused by H 2 O 2 and decrease the levels of NF-κB p65, NLRP3, TNF-α, Beclin1, LC3, and P62 proteins. Additionally, there seems to be a targeting relationship between SAL and EZH2, and EZH2 knockdown can reproduce the protective effect of SAL on endothelial function. Overall, ...