Aspirin Eugenol Ester Reduces H2O2-Induced Oxidative Stress of HUVECs via Mitochondria-Lysosome Axis
Identifieur interne : 000A60 ( Main/Exploration ); précédent : 000A59; suivant : 000A61Aspirin Eugenol Ester Reduces H2O2-Induced Oxidative Stress of HUVECs via Mitochondria-Lysosome Axis
Auteurs : Mei-Zhou Huang [République populaire de Chine] ; Ya-Jun Yang [République populaire de Chine] ; Xi-Wang Liu [République populaire de Chine] ; Zhe Qin [République populaire de Chine] ; Jian-Yong Li [République populaire de Chine]Source :
- Oxidative Medicine and Cellular Longevity [ 1942-0900 ] ; 2019.
Abstract
The oxidative stress of vessel endothelium is a major risk factor of cardiovascular disorders. Antioxidative stress drugs are widely used in cardiovascular therapy. Aspirin eugenol ester (AEE) is a new pharmaceutical compound synthesized by esterification reaction of aspirin with eugenols and possesses antioxidative activity. The present study was designed to investigate the mechanism how AEE protects human umbilical vein endothelial cells (HUVECs) from H2O2-induced oxidative stress. H2O2 was given to the HUVECs with or without AEE pretreatment. Changes in the oxidative stress-related factors, including those related to the mitochondria-lysosome axis, were determined with Western blotting, cellular immunofluorescence, and enzyme activity test. The results showed that, in the HUVECs, 300
Url:
DOI: 10.1155/2019/8098135
PubMed: 31583045
PubMed Central: 6754946
Affiliations:
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Aspirin Eugenol Ester Reduces H<sub>2</sub>
O<sub>2</sub>
-Induced Oxidative Stress of HUVECs via Mitochondria-Lysosome Axis</title>
<author><name sortKey="Huang, Mei Zhou" sort="Huang, Mei Zhou" uniqKey="Huang M" first="Mei-Zhou" last="Huang">Mei-Zhou Huang</name>
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<country xml:lang="fr">République populaire de Chine</country>
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</affiliation>
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<author><name sortKey="Yang, Ya Jun" sort="Yang, Ya Jun" uniqKey="Yang Y" first="Ya-Jun" last="Yang">Ya-Jun Yang</name>
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<country xml:lang="fr">République populaire de Chine</country>
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<author><name sortKey="Liu, Xi Wang" sort="Liu, Xi Wang" uniqKey="Liu X" first="Xi-Wang" last="Liu">Xi-Wang Liu</name>
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<author><name sortKey="Qin, Zhe" sort="Qin, Zhe" uniqKey="Qin Z" first="Zhe" last="Qin">Zhe Qin</name>
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<author><name sortKey="Li, Jian Yong" sort="Li, Jian Yong" uniqKey="Li J" first="Jian-Yong" last="Li">Jian-Yong Li</name>
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<series><title level="j">Oxidative Medicine and Cellular Longevity</title>
<idno type="ISSN">1942-0900</idno>
<idno type="eISSN">1942-0994</idno>
<imprint><date when="2019">2019</date>
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<front><div type="abstract" xml:lang="en"><p>The oxidative stress of vessel endothelium is a major risk factor of cardiovascular disorders. Antioxidative stress drugs are widely used in cardiovascular therapy. Aspirin eugenol ester (AEE) is a new pharmaceutical compound synthesized by esterification reaction of aspirin with eugenols and possesses antioxidative activity. The present study was designed to investigate the mechanism how AEE protects human umbilical vein endothelial cells (HUVECs) from H<sub>2</sub>
O<sub>2</sub>
-induced oxidative stress. H<sub>2</sub>
O<sub>2</sub>
was given to the HUVECs with or without AEE pretreatment. Changes in the oxidative stress-related factors, including those related to the mitochondria-lysosome axis, were determined with Western blotting, cellular immunofluorescence, and enzyme activity test. The results showed that, in the HUVECs, 300 <italic>μ</italic>
M H<sub>2</sub>
O<sub>2</sub>
treatment significantly increased the apoptosis rate, MDA concentration, reactive oxygen species (ROS) production, mitochondrial membrane potential, expression of Bax and mature cathepsin D (CTSD), and activity of CTSD and Caspase3 (Cas3) but decreased the expression of Bcl2 and lysosomal membrane stability, while in the HUVECs pretreated with AEE, the above changes caused by either the stimulatory or the inhibitory effect of H<sub>2</sub>
O<sub>2</sub>
on the relevant factors were significantly reduced. AEE pretreatment significantly enhanced the activity of cellular superoxide dismutase and glutathione peroxidase in the HUVECs. Our findings suggest that AEE effectively reduced H<sub>2</sub>
O<sub>2</sub>
-induced oxidative stress in the HUVECs via mitochondria-lysosome axis.</p>
</div>
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<affiliations><list><country><li>République populaire de Chine</li>
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<tree><country name="République populaire de Chine"><noRegion><name sortKey="Huang, Mei Zhou" sort="Huang, Mei Zhou" uniqKey="Huang M" first="Mei-Zhou" last="Huang">Mei-Zhou Huang</name>
</noRegion>
<name sortKey="Li, Jian Yong" sort="Li, Jian Yong" uniqKey="Li J" first="Jian-Yong" last="Li">Jian-Yong Li</name>
<name sortKey="Liu, Xi Wang" sort="Liu, Xi Wang" uniqKey="Liu X" first="Xi-Wang" last="Liu">Xi-Wang Liu</name>
<name sortKey="Qin, Zhe" sort="Qin, Zhe" uniqKey="Qin Z" first="Zhe" last="Qin">Zhe Qin</name>
<name sortKey="Yang, Ya Jun" sort="Yang, Ya Jun" uniqKey="Yang Y" first="Ya-Jun" last="Yang">Ya-Jun Yang</name>
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