SAL protects endothelial cells from H 2 O 2 -induced endothelial dysfunction: Regulation of inflammation and autophagy by EZH2.

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, SAL inhibits H ₂ O ₂ -induced HUVEC dysfunction by regulating autophagy and inflammatory signaling pathways through EZH2.
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