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image of HYQTD Drug-containing Serum Alleviates H2O2-induced Endothelial Oxidative Damage by Increasing Mitochondrial ATP Synthesis and Inhibiting ROS

Abstract

Background

Atherosclerosis (AS) is caused by the endothelium injury associated with oxidative stress. Previous studies have shown that the Phlegm-Eliminating and Stasis-Transforming Decoction (Huayu Qutan Decoction, HYQTD) has mitochondrial protective function. The objective of this research was to explore how HYQTD drug-containing serum (HYQTD-DS) could potentially protect mitochondrial energy production in endothelial cells (ECs) from injury caused by hydrogen peroxide (HO)-induced oxidative damage in AS through SIRT1/PGC-1α/ Nrf2 pathway.

Methods

After preparation of containing serum, the cells were divided into various categories, such as control group, HO group (an oxidative damage model), HYQTD group, Selisistat (EX527, a SIRT1 inhibitor) combined with HO group, and EX527 combined with HYQTD group. The evaluation of oxidative stress involved measuring reactive oxygen species (ROS) and malondialdehyde (MDA) generation, as well as Superoxide Dismutase (SOD) activity. Mitochondrial function and ultrastructure were measured by Transmission electron microscopy (TEM), mitochondrial membrane potential (MMP), rate of oxygen consumption (OCR), respiratory chain complex activities, and ATP production. The key proteins and gene levels in the SIRT1/PGC-1α/Nrf2 pathway was quantified by quantitative real-time PCR (RT-PCR) and Western blotting analysis.

Results

We found oxidative stress, mitochondrial damage, and mitochondrial energy disorder in HO-induced ECs. However it indicated a marked reversal after pretreated with HYQTD-DS. Mechanistically, EX527 induced increased oxidative stress, worse mitochondrial dysfunction, and less ATP synthesis.

Conclusion

We demonstrated that HYQTD-DS attenuated oxidative stress, improved mitochondrial function, and up-regulated mitochondrial ATP synthesis by activating SIRT1/PGC-1α/Nrf2 pathway-induced mitochondrial biogenesis and its downstream NADH dehydrogenase (ubiquinone) flavoprotein 2 (NDV2).

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2025-01-27
2025-03-26

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HYQTD Drug-containing Serum Alleviates H2O2-induced Endothelial Oxidative Damage by Increasing Mitochondrial ATP Synthesis and Inhibiting ROS
Bentham Science Publishers ; https://doi.org/10.2174/0113892010333981250122003904
/content/journals/cpb/10.2174/0113892010333981250122003904
/content/journals/cpb/10.2174/0113892010333981250122003904
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  • Article Type:     Research Article
Keywords: vascular endothelial injury ; oxidative stress ; mitochondrial ATP synthesis ; Traditional Chinese medicine

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