Aspirin Eugenol Ester Reduces H2O2-Induced Oxidative Stress of HUVECs via Mitochondria-Lysosome Axis
Identifieur interne : 000761 ( Pmc/Curation ); précédent : 000760; suivant : 000762Aspirin 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
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DOI: 10.1155/2019/8098135
PubMed: 31583045
PubMed Central: 6754946
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">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><affiliation wicri:level="1"><nlm:aff id="I1">Key Lab of New Animal Drug Project of Gansu Province, Key Lab of Veterinary Pharmaceutical Development of Ministry of Agriculture, Lanzhou Institute of Husbandry and Pharmaceutical Sciences of CAAS, Lanzhou 730050, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Key Lab of New Animal Drug Project of Gansu Province, Key Lab of Veterinary Pharmaceutical Development of Ministry of Agriculture, Lanzhou Institute of Husbandry and Pharmaceutical Sciences of CAAS, Lanzhou 730050</wicri:regionArea></affiliation></author><author><name sortKey="Yang, Ya Jun" sort="Yang, Ya Jun" uniqKey="Yang Y" first="Ya-Jun" last="Yang">Ya-Jun Yang</name><affiliation wicri:level="1"><nlm:aff id="I1">Key Lab of New Animal Drug Project of Gansu Province, Key Lab of Veterinary Pharmaceutical Development of Ministry of Agriculture, Lanzhou Institute of Husbandry and Pharmaceutical Sciences of CAAS, Lanzhou 730050, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Key Lab of New Animal Drug Project of Gansu Province, Key Lab of Veterinary Pharmaceutical Development of Ministry of Agriculture, Lanzhou Institute of Husbandry and Pharmaceutical Sciences of CAAS, Lanzhou 730050</wicri:regionArea></affiliation></author><author><name sortKey="Liu, Xi Wang" sort="Liu, Xi Wang" uniqKey="Liu X" first="Xi-Wang" last="Liu">Xi-Wang Liu</name><affiliation wicri:level="1"><nlm:aff id="I1">Key Lab of New Animal Drug Project of Gansu Province, Key Lab of Veterinary Pharmaceutical Development of Ministry of Agriculture, Lanzhou Institute of Husbandry and Pharmaceutical Sciences of CAAS, Lanzhou 730050, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Key Lab of New Animal Drug Project of Gansu Province, Key Lab of Veterinary Pharmaceutical Development of Ministry of Agriculture, Lanzhou Institute of Husbandry and Pharmaceutical Sciences of CAAS, Lanzhou 730050</wicri:regionArea></affiliation></author><author><name sortKey="Qin, Zhe" sort="Qin, Zhe" uniqKey="Qin Z" first="Zhe" last="Qin">Zhe Qin</name><affiliation wicri:level="1"><nlm:aff id="I1">Key Lab of New Animal Drug Project of Gansu Province, Key Lab of Veterinary Pharmaceutical Development of Ministry of Agriculture, Lanzhou Institute of Husbandry and Pharmaceutical Sciences of CAAS, Lanzhou 730050, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Key Lab of New Animal Drug Project of Gansu Province, Key Lab of Veterinary Pharmaceutical Development of Ministry of Agriculture, Lanzhou Institute of Husbandry and Pharmaceutical Sciences of CAAS, Lanzhou 730050</wicri:regionArea></affiliation></author><author><name sortKey="Li, Jian Yong" sort="Li, Jian Yong" uniqKey="Li J" first="Jian-Yong" last="Li">Jian-Yong Li</name><affiliation wicri:level="1"><nlm:aff id="I1">Key Lab of New Animal Drug Project of Gansu Province, Key Lab of Veterinary Pharmaceutical Development of Ministry of Agriculture, Lanzhou Institute of Husbandry and Pharmaceutical Sciences of CAAS, Lanzhou 730050, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Key Lab of New Animal Drug Project of Gansu Province, Key Lab of Veterinary Pharmaceutical Development of Ministry of Agriculture, Lanzhou Institute of Husbandry and Pharmaceutical Sciences of CAAS, Lanzhou 730050</wicri:regionArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">31583045</idno><idno type="pmc">6754946</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6754946</idno><idno type="RBID">PMC:6754946</idno><idno type="doi">10.1155/2019/8098135</idno><date when="2019">2019</date><idno type="wicri:Area/Pmc/Corpus">000761</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000761</idno><idno type="wicri:Area/Pmc/Curation">000761</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000761</idno></publicationStmt><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><affiliation wicri:level="1"><nlm:aff id="I1">Key Lab of New Animal Drug Project of Gansu Province, Key Lab of Veterinary Pharmaceutical Development of Ministry of Agriculture, Lanzhou Institute of Husbandry and Pharmaceutical Sciences of CAAS, Lanzhou 730050, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Key Lab of New Animal Drug Project of Gansu Province, Key Lab of Veterinary Pharmaceutical Development of Ministry of Agriculture, Lanzhou Institute of Husbandry and Pharmaceutical Sciences of CAAS, Lanzhou 730050</wicri:regionArea></affiliation></author><author><name sortKey="Yang, Ya Jun" sort="Yang, Ya Jun" uniqKey="Yang Y" first="Ya-Jun" last="Yang">Ya-Jun Yang</name><affiliation wicri:level="1"><nlm:aff id="I1">Key Lab of New Animal Drug Project of Gansu Province, Key Lab of Veterinary Pharmaceutical Development of Ministry of Agriculture, Lanzhou Institute of Husbandry and Pharmaceutical Sciences of CAAS, Lanzhou 730050, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Key Lab of New Animal Drug Project of Gansu Province, Key Lab of Veterinary Pharmaceutical Development of Ministry of Agriculture, Lanzhou Institute of Husbandry and Pharmaceutical Sciences of CAAS, Lanzhou 730050</wicri:regionArea></affiliation></author><author><name sortKey="Liu, Xi Wang" sort="Liu, Xi Wang" uniqKey="Liu X" first="Xi-Wang" last="Liu">Xi-Wang Liu</name><affiliation wicri:level="1"><nlm:aff id="I1">Key Lab of New Animal Drug Project of Gansu Province, Key Lab of Veterinary Pharmaceutical Development of Ministry of Agriculture, Lanzhou Institute of Husbandry and Pharmaceutical Sciences of CAAS, Lanzhou 730050, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Key Lab of New Animal Drug Project of Gansu Province, Key Lab of Veterinary Pharmaceutical Development of Ministry of Agriculture, Lanzhou Institute of Husbandry and Pharmaceutical Sciences of CAAS, Lanzhou 730050</wicri:regionArea></affiliation></author><author><name sortKey="Qin, Zhe" sort="Qin, Zhe" uniqKey="Qin Z" first="Zhe" last="Qin">Zhe Qin</name><affiliation wicri:level="1"><nlm:aff id="I1">Key Lab of New Animal Drug Project of Gansu Province, Key Lab of Veterinary Pharmaceutical Development of Ministry of Agriculture, Lanzhou Institute of Husbandry and Pharmaceutical Sciences of CAAS, Lanzhou 730050, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Key Lab of New Animal Drug Project of Gansu Province, Key Lab of Veterinary Pharmaceutical Development of Ministry of Agriculture, Lanzhou Institute of Husbandry and Pharmaceutical Sciences of CAAS, Lanzhou 730050</wicri:regionArea></affiliation></author><author><name sortKey="Li, Jian Yong" sort="Li, Jian Yong" uniqKey="Li J" first="Jian-Yong" last="Li">Jian-Yong Li</name><affiliation wicri:level="1"><nlm:aff id="I1">Key Lab of New Animal Drug Project of Gansu Province, Key Lab of Veterinary Pharmaceutical Development of Ministry of Agriculture, Lanzhou Institute of Husbandry and Pharmaceutical Sciences of CAAS, Lanzhou 730050, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Key Lab of New Animal Drug Project of Gansu Province, Key Lab of Veterinary Pharmaceutical Development of Ministry of Agriculture, Lanzhou Institute of Husbandry and Pharmaceutical Sciences of CAAS, Lanzhou 730050</wicri:regionArea></affiliation></author></analytic><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></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><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></front><back><div1 type="bibliography"><listBibl><biblStruct></biblStruct><biblStruct><analytic><author><name sortKey="Tikkanen, E" uniqKey="Tikkanen E">E. Tikkanen</name></author><author><name sortKey="Gustafsson, S" uniqKey="Gustafsson S">S. Gustafsson</name></author><author><name sortKey="Ingelsson, E" uniqKey="Ingelsson E">E. Ingelsson</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Roever, L" uniqKey="Roever L">L. Roever</name></author><author><name sortKey="Tse, G" uniqKey="Tse G">G. Tse</name></author><author><name sortKey="Biondi Zoccai, G" uniqKey="Biondi Zoccai G">G. Biondi-Zoccai</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Cai, H" uniqKey="Cai H">H. Cai</name></author><author><name sortKey="Harrison, D G" uniqKey="Harrison D">D. G. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Oxid Med Cell Longev</journal-id><journal-id journal-id-type="iso-abbrev">Oxid Med Cell Longev</journal-id><journal-id journal-id-type="publisher-id">OMCL</journal-id><journal-title-group><journal-title>Oxidative Medicine and Cellular Longevity</journal-title></journal-title-group><issn pub-type="ppub">1942-0900</issn><issn pub-type="epub">1942-0994</issn><publisher><publisher-name>Hindawi</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">31583045</article-id><article-id pub-id-type="pmc">6754946</article-id><article-id pub-id-type="doi">10.1155/2019/8098135</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group></article-categories><title-group><article-title>Aspirin Eugenol Ester Reduces H<sub>2</sub>O<sub>2</sub>-Induced Oxidative Stress of HUVECs via Mitochondria-Lysosome Axis</article-title></title-group><contrib-group><contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="false">https://orcid.org/0000-0003-2538-0217</contrib-id><name><surname>Huang</surname><given-names>Mei-Zhou</given-names></name><xref ref-type="aff" rid="I1"></xref></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="false">https://orcid.org/0000-0001-9651-8549</contrib-id><name><surname>Yang</surname><given-names>Ya-Jun</given-names></name><xref ref-type="aff" rid="I1"></xref></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="false">https://orcid.org/0000-0002-1623-0308</contrib-id><name><surname>Liu</surname><given-names>Xi-Wang</given-names></name><xref ref-type="aff" rid="I1"></xref></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="false">https://orcid.org/0000-0001-5417-5285</contrib-id><name><surname>Qin</surname><given-names>Zhe</given-names></name><xref ref-type="aff" rid="I1"></xref></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid" authenticated="false">https://orcid.org/0000-0003-3317-0666</contrib-id><name><surname>Li</surname><given-names>Jian-Yong</given-names></name><email>lijy1971@163.com</email><xref ref-type="aff" rid="I1"></xref></contrib></contrib-group><aff id="I1">Key Lab of New Animal Drug Project of Gansu Province, Key Lab of Veterinary Pharmaceutical Development of Ministry of Agriculture, Lanzhou Institute of Husbandry and Pharmaceutical Sciences of CAAS, Lanzhou 730050, China</aff><author-notes><fn fn-type="other"><p>Academic Editor: Maria R. Ciriolo</p></fn></author-notes><pub-date pub-type="collection"><year>2019</year></pub-date><pub-date pub-type="epub"><day>9</day><month>9</month><year>2019</year></pub-date><volume>2019</volume><elocation-id>8098135</elocation-id><history><date date-type="received"><day>14</day><month>10</month><year>2018</year></date><date date-type="rev-recd"><day>12</day><month>3</month><year>2019</year></date><date date-type="accepted"><day>7</day><month>4</month><year>2019</year></date></history><permissions><copyright-statement>Copyright © 2019 Mei-Zhou Huang et al.</copyright-statement><copyright-year>2019</copyright-year><license xlink:href="http://creativecommons.org/licenses/by/4.0/"><license-p>This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</license-p></license></permissions><abstract><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></abstract><funding-group><award-group><funding-source>National Natural Science Foundation of China</funding-source><award-id>31872518</award-id><award-id>31572573</award-id></award-group></funding-group></article-meta></front><floats-group><fig id="fig1" orientation="portrait" position="float"><label>Figure 1</label><caption><p>AEE reduced the apoptosis of HUVECs induced by H<sub>2</sub>O<sub>2</sub>. (a) The double stained with Annexin V and PI results among different treatment groups. (b) The apoptosis rate among different treatment groups. Values were expressed as mean ± SD, <italic>n</italic> = 6; <sup>∗</sup><italic>p</italic> < 0.05, compared with the normal group; <sup>#</sup><italic>p</italic> < 0.05, compared with the group treated with H<sub>2</sub>O<sub>2</sub> alone (one-way ANOVA followed with Duncan's multiple comparisons).</p></caption><graphic xlink:href="OMCL2019-8098135.001"></graphic></fig><fig id="fig2" orientation="portrait" position="float"><label>Figure 2</label><caption><p>AEE enhanced the antioxidant capacity of HUVECs. (a) AEE decreased lipid peroxidation in the HUVECs. (b) AEE enhanced the SOD activity. (c) AEE raised the GSH-Px activity. (d) AEE increased the ratio of GSH to GSSG. Values were expressed as mean ± SD, <italic>n</italic> = 6; <sup>∗</sup><italic>p</italic> < 0.05, compared with the normal group; <sup>#</sup><italic>p</italic> < 0.05, compared with the group treated with H<sub>2</sub>O<sub>2</sub> alone (one-way ANOVA followed with Duncan's multiple comparisons).</p></caption><graphic xlink:href="OMCL2019-8098135.002"></graphic></fig><fig id="fig3" orientation="portrait" position="float"><label>Figure 3</label><caption><p>AEE ameliorated lysosomal disorder induced by H<sub>2</sub>O<sub>2</sub>. (a, b) AEE reduced the expression of mature CTSD induced by H<sub>2</sub>O<sub>2</sub>. (c) AEE reduced the increase in CTSD activity induced by H<sub>2</sub>O<sub>2</sub>. The high-density fluorescence of LysoTracker Red was indicated by green arrows. (d, e) AEE enhanced the stability of the lysosomal membrane disrupted by H<sub>2</sub>O<sub>2</sub> ((d) 10 × 40 power). “+” including the treatment in the HUVECs; “-”excluding the treatment on the HUVECs. Values are expressed as mean ± SD, <italic>n</italic> = 6; <sup>∗</sup><italic>p</italic> < 0.05, compared with the normal group; <sup>#</sup><italic>p</italic> < 0.05, compared with the group of H<sub>2</sub>O<sub>2</sub> alone (one-way ANOVA followed with Duncan's multiple comparisons).</p></caption><graphic xlink:href="OMCL2019-8098135.003"></graphic></fig><fig id="fig4" orientation="portrait" position="float"><label>Figure 4</label><caption><p>AEE alleviated the mitochondrial dysfunction induced by H<sub>2</sub>O<sub>2</sub>. (a, b) AEE reduced the collapse of the mitochondrial membrane potential induced by H<sub>2</sub>O<sub>2</sub> ((a) 10 × 40 power). (c, d) AEE reduced the generation of cellular and mitochondrial ROS induced by H<sub>2</sub>O<sub>2</sub> (upper part of (c): 10 × 10 power; lower part of (c): 10 × 40 power); “+” with the treatment in the HUVECs, “-” excluding the treatment on the HUVECs. (e, f) AEE prevented the release of Cyt c from mitochondria ((e) 10 × 40 power). Values are expressed as mean ± SD, <italic>n</italic> = 6; <sup>∗</sup><italic>p</italic> < 0.05, compared with the normal group; <sup>#</sup><italic>p</italic> < 0.05, compared with the group of H<sub>2</sub>O<sub>2</sub> alone (one-way ANOVA followed with Duncan's multiple comparisons).</p></caption><graphic xlink:href="OMCL2019-8098135.004"></graphic></fig><fig id="fig5" orientation="portrait" position="float"><label>Figure 5</label><caption><p>AEE treatment reduced the effect of H<sub>2</sub>O<sub>2</sub> on antiapoptosis or proapoptosis proteins. (a, b) AEE reduced H<sub>2</sub>O<sub>2</sub>-induced expression of mature Cas3 and Bid and reversed the H<sub>2</sub>O<sub>2</sub>-inhibited expression of Bcl2 and Bcl-XL. (c, d) AEE reduced H<sub>2</sub>O<sub>2</sub>-induced expression of Bax ((c) 10 × 40 power). “+” with the treatment in the HUVECs; “-” without the treatment in the HUVECs. Values are expressed as mean ± SD, <italic>n</italic> = 6; <sup>∗</sup><italic>p</italic> < 0.05, compared with the normal group; <sup>#</sup><italic>p</italic> < 0.05, compared with the group of H<sub>2</sub>O<sub>2</sub> alone.</p></caption><graphic xlink:href="OMCL2019-8098135.005"></graphic></fig><fig id="fig6" orientation="portrait" position="float"><label>Figure 6</label><caption><p>Genetic inhibition of Bcl2 reduced the effect of AEE on H<sub>2</sub>O<sub>2</sub>-induced mitochondrial and lysosomal dysfunction. (a, b) The changes in the mitochondrial membrane potential between different treatment groups ((a) 10 × 40 power). (c, d) The changes in ROS production between different treatment groups ((c) 10 × 40 power). (e, f) The changes in CTSD and Cas3 activity among different treatment groups. “+” with the treatment in the HUVECs; “-” without the treatment in the HUVECs. Values are expressed as mean ± SD, <italic>n</italic> = 6; <sup>∗</sup><italic>p</italic> < 0.05, compared with the group of overexpression alone; <sup>#</sup><italic>p</italic> < 0.05, compared with the group of H<sub>2</sub>O<sub>2</sub> alone (one-way ANOVA followed with Duncan's multiple comparisons).</p></caption><graphic xlink:href="OMCL2019-8098135.006"></graphic></fig></floats-group></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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