Proanthocyanidins Antagonize Arsenic-Induced Oxidative Damage and Promote Arsenic Methylation through Activation of the Nrf2 Signaling Pathway

Purpose. To investigate the effects of grape seed proanthocyanidin extract (GSPE) on oxidative damage and arsenic (As) methylation and to clarify the role of Nrf2 in the process. Methods. L-02 cells were treated with arsenic (25 μM) and GSPE (10, 25, and 50 mg/L) for 24 h. Cell viability was analyze...

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Published in:Oxidative medicine and cellular longevity 2019, Vol.2019 (2019), p.1-19
Main Authors: Wang, Hai-Xia, Feng, Gangling, Hu, Yun-Hua, Niu, Qiang, Xu, Meng-Chuan, Li, Shugang
Format: Article
Language:English
Subjects:
Animals
Antioxidants
Apoptosis
Arsenic
Arsenic - toxicity
Cell Line
Cell Survival - drug effects
Cytotoxicity
Enzymes
Free radicals
Grape Seed Extract - pharmacology
Lipid peroxidation
Liver
Liver - drug effects
Liver - pathology
Liver - physiopathology
Metabolism
Methylation
NF-E2-Related Factor 2 - genetics
NF-E2-Related Factor 2 - metabolism
Oxidative stress
Oxidative Stress - drug effects
Penicillin
Poisoning
Proanthocyanidins - pharmacology
Proteomics
R&D
Reactive Oxygen Species - metabolism
Research & development
RNA, Messenger - genetics
RNA, Messenger - metabolism
Rodents
Signal Transduction - drug effects
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Feng, Gangling
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Li, Shugang
description Purpose. To investigate the effects of grape seed proanthocyanidin extract (GSPE) on oxidative damage and arsenic (As) methylation and to clarify the role of Nrf2 in the process. Methods. L-02 cells were treated with arsenic (25 μM) and GSPE (10, 25, and 50 mg/L) for 24 h. Cell viability was analyzed by MTT assay. Cell apoptosis and ROS fluorescence were detected by flow cytometry. Oxidative stress marker levels were measured using commercial kits. mRNA and protein expression were detected by qRT-PCR and western blotting. The cellular concentrations of methylation products were measured by HPLC-HGAFS. Arsenic methylation ability of cells was determined. Results. Cell survival rate was significantly lower in the As group than in the control group (P
doi_str_mv 10.1155/2019/8549035
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To investigate the effects of grape seed proanthocyanidin extract (GSPE) on oxidative damage and arsenic (As) methylation and to clarify the role of Nrf2 in the process. Methods. L-02 cells were treated with arsenic (25 μM) and GSPE (10, 25, and 50 mg/L) for 24 h. Cell viability was analyzed by MTT assay. Cell apoptosis and ROS fluorescence were detected by flow cytometry. Oxidative stress marker levels were measured using commercial kits. mRNA and protein expression were detected by qRT-PCR and western blotting. The cellular concentrations of methylation products were measured by HPLC-HGAFS. Arsenic methylation ability of cells was determined. Results. Cell survival rate was significantly lower in the As group than in the control group (P&lt;0.05), while cell apoptosis increased and the number of apoptotic cells decreased gradually after GSPE intervention. Superoxide dismutase, glutathione, and sulfhydryl levels in the intervention group were significantly higher (P&lt;0.05), while MDA and ROS levels were significantly lower (P&lt;0.05) than those in the As group. The mRNA and protein expression of Nrf2, HO-1, NQO1, and glutathione-S-transferase increased in the As + GSPE group compared with that in the As group (P&lt;0.05). GSPE significantly increased methylated As level, primary methylation index, secondary methylation index, average growth rate of methylation, and average methylation speed compared with the GSPE untreated group (P&lt;0.05). After Nrf2 inhibition, the effect of GSPE decreased significantly. Conclusion. GSPE activates the Nrf2 signaling pathway to antagonize As-induced oxidative damage and to promote As methylation metabolism. Therefore, GSPE may be a potential agent for relieving As-induced hepatotoxicity.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2019/8549035</identifier><identifier>PMID: 30805085</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Animals ; Antioxidants ; Apoptosis ; Arsenic ; Arsenic - toxicity ; Cell Line ; Cell Survival - drug effects ; Cytotoxicity ; Enzymes ; Free radicals ; Grape Seed Extract - pharmacology ; Lipid peroxidation ; Liver ; Liver - drug effects ; Liver - pathology ; Liver - physiopathology ; Metabolism ; Methylation ; NF-E2-Related Factor 2 - genetics ; NF-E2-Related Factor 2 - metabolism ; Oxidative stress ; Oxidative Stress - drug effects ; Penicillin ; Poisoning ; Proanthocyanidins - pharmacology ; Proteomics ; R&amp;D ; Reactive Oxygen Species - metabolism ; Research &amp; development ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Rodents ; Signal Transduction - drug effects</subject><ispartof>Oxidative medicine and cellular longevity, 2019, Vol.2019 (2019), p.1-19</ispartof><rights>Copyright © 2019 Mengchuan Xu et al.</rights><rights>Copyright © 2019 Mengchuan Xu et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. http://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2019 Mengchuan Xu et al. 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3865-85f3be63a06503f4308b6b945dd747ac392373f701e8717f400fd7149a53c2e13</citedby><cites>FETCH-LOGICAL-c3865-85f3be63a06503f4308b6b945dd747ac392373f701e8717f400fd7149a53c2e13</cites><orcidid>0000-0002-9278-6412 ; 0000-0001-6162-7438</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2175231804/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2175231804?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,780,784,885,4024,25753,27923,27924,27925,37012,44590,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30805085$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Mahmoud, Ayman M.</contributor><contributor>Ayman M Mahmoud</contributor><creatorcontrib>Wang, Hai-Xia</creatorcontrib><creatorcontrib>Feng, Gangling</creatorcontrib><creatorcontrib>Hu, Yun-Hua</creatorcontrib><creatorcontrib>Niu, Qiang</creatorcontrib><creatorcontrib>Xu, Meng-Chuan</creatorcontrib><creatorcontrib>Li, Shugang</creatorcontrib><title>Proanthocyanidins Antagonize Arsenic-Induced Oxidative Damage and Promote Arsenic Methylation through Activation of the Nrf2 Signaling Pathway</title><title>Oxidative medicine and cellular longevity</title><addtitle>Oxid Med Cell Longev</addtitle><description>Purpose. To investigate the effects of grape seed proanthocyanidin extract (GSPE) on oxidative damage and arsenic (As) methylation and to clarify the role of Nrf2 in the process. Methods. L-02 cells were treated with arsenic (25 μM) and GSPE (10, 25, and 50 mg/L) for 24 h. Cell viability was analyzed by MTT assay. Cell apoptosis and ROS fluorescence were detected by flow cytometry. Oxidative stress marker levels were measured using commercial kits. mRNA and protein expression were detected by qRT-PCR and western blotting. The cellular concentrations of methylation products were measured by HPLC-HGAFS. Arsenic methylation ability of cells was determined. Results. Cell survival rate was significantly lower in the As group than in the control group (P&lt;0.05), while cell apoptosis increased and the number of apoptotic cells decreased gradually after GSPE intervention. Superoxide dismutase, glutathione, and sulfhydryl levels in the intervention group were significantly higher (P&lt;0.05), while MDA and ROS levels were significantly lower (P&lt;0.05) than those in the As group. The mRNA and protein expression of Nrf2, HO-1, NQO1, and glutathione-S-transferase increased in the As + GSPE group compared with that in the As group (P&lt;0.05). GSPE significantly increased methylated As level, primary methylation index, secondary methylation index, average growth rate of methylation, and average methylation speed compared with the GSPE untreated group (P&lt;0.05). After Nrf2 inhibition, the effect of GSPE decreased significantly. Conclusion. GSPE activates the Nrf2 signaling pathway to antagonize As-induced oxidative damage and to promote As methylation metabolism. 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To investigate the effects of grape seed proanthocyanidin extract (GSPE) on oxidative damage and arsenic (As) methylation and to clarify the role of Nrf2 in the process. Methods. L-02 cells were treated with arsenic (25 μM) and GSPE (10, 25, and 50 mg/L) for 24 h. Cell viability was analyzed by MTT assay. Cell apoptosis and ROS fluorescence were detected by flow cytometry. Oxidative stress marker levels were measured using commercial kits. mRNA and protein expression were detected by qRT-PCR and western blotting. The cellular concentrations of methylation products were measured by HPLC-HGAFS. Arsenic methylation ability of cells was determined. Results. Cell survival rate was significantly lower in the As group than in the control group (P&lt;0.05), while cell apoptosis increased and the number of apoptotic cells decreased gradually after GSPE intervention. Superoxide dismutase, glutathione, and sulfhydryl levels in the intervention group were significantly higher (P&lt;0.05), while MDA and ROS levels were significantly lower (P&lt;0.05) than those in the As group. The mRNA and protein expression of Nrf2, HO-1, NQO1, and glutathione-S-transferase increased in the As + GSPE group compared with that in the As group (P&lt;0.05). GSPE significantly increased methylated As level, primary methylation index, secondary methylation index, average growth rate of methylation, and average methylation speed compared with the GSPE untreated group (P&lt;0.05). After Nrf2 inhibition, the effect of GSPE decreased significantly. Conclusion. GSPE activates the Nrf2 signaling pathway to antagonize As-induced oxidative damage and to promote As methylation metabolism. Therefore, GSPE may be a potential agent for relieving As-induced hepatotoxicity.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>30805085</pmid><doi>10.1155/2019/8549035</doi><tpages>19</tpages><orcidid>https://orcid.org/0000-0002-9278-6412</orcidid><orcidid>https://orcid.org/0000-0001-6162-7438</orcidid><oa>free_for_read</oa></addata></record>
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subjects Animals
Antioxidants
Apoptosis
Arsenic
Arsenic - toxicity
Cell Line
Cell Survival - drug effects
Cytotoxicity
Enzymes
Free radicals
Grape Seed Extract - pharmacology
Lipid peroxidation
Liver
Liver - drug effects
Liver - pathology
Liver - physiopathology
Metabolism
Methylation
NF-E2-Related Factor 2 - genetics
NF-E2-Related Factor 2 - metabolism
Oxidative stress
Oxidative Stress - drug effects
Penicillin
Poisoning
Proanthocyanidins - pharmacology
Proteomics
R&D
Reactive Oxygen Species - metabolism
Research & development
RNA, Messenger - genetics
RNA, Messenger - metabolism
Rodents
Signal Transduction - drug effects
title Proanthocyanidins Antagonize Arsenic-Induced Oxidative Damage and Promote Arsenic Methylation through Activation of the Nrf2 Signaling Pathway
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