Protective Effect of Piceatannol Against Cerebral Ischaemia–Reperfusion Injury Via Regulating Nrf2/HO-1 Pathway In Vivo and Vitro
Piceatannol is a natural plant-derived compound with protective effects against cardiovascular diseases. However, its effect on cerebral ischaemia–reperfusion injury (CIRI) induced by oxidative stress remains unclear. This study aimed to investigate piceatannol’s antioxidation in CIRI. An in vitro o...
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| Veröffentlicht in: | Neurochemical research 2021-07, Vol.46 (7), p.1869-1880 |
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| creator | Wang, Lingfeng Guo, Ying Ye, Jiayi Pan, Zeyue Hu, Peihao Zhong, Xiaoming Qiu, Fengmei Zhang, Danni Huang, Zhen |
| description | Piceatannol is a natural plant-derived compound with protective effects against cardiovascular diseases. However, its effect on cerebral ischaemia–reperfusion injury (CIRI) induced by oxidative stress remains unclear. This study aimed to investigate piceatannol’s antioxidation in CIRI. An in vitro oxygen–glucose deprivation followed by reoxygenation model was used and cell viability was measured. A middle cerebral artery occlusion followed by reperfusion model was used in vivo. Neurological function, encephalisation quotient, oedema, and volume of the cerebral infarction were then evaluated. The effects of piceatannol on histopathological findings, as well as the ultrastructure of the cortex, were analysed. The activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and lactate dehydrogenase (LDH) and the malondialdehyde (MDA) content was measured both in vitro and in vivo. Finally, the expression of nuclear factor erythroid-2-related factor 2 (Nrf2), hemeoxygenase-1 (HO-1), and nicotinamide adenine dinucleotide phosphate quinone oxidoreductase 1 (NQO1) in cerebral tissue was detected using reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blotting. Our results demonstrated that cell viability in the piceatannol groups was increased. The SOD, GSH-Px activities were increased as LDH activity and MDA content decreased in the piceatannol groups both in vitro and in vivo, reflecting a decrease in oxidative stress. The neurological severity score and infarction volume in the piceatannol groups at doses of 10 and 20 mg/kg were lower than those of the model group. Furthermore, the damage seen on histopathological examination was partially attenuated by piceatannol. RT-qPCR and western blot analysis indicated that the expression of Nrf2, HO-1, and NQO1 were significantly increased by piceatannol. The results of the study demonstrate that piceatannol exerts a protective effect against CIRI. |
| doi_str_mv | 10.1007/s11064-021-03328-8 |
| format | Article |
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However, its effect on cerebral ischaemia–reperfusion injury (CIRI) induced by oxidative stress remains unclear. This study aimed to investigate piceatannol’s antioxidation in CIRI. An in vitro oxygen–glucose deprivation followed by reoxygenation model was used and cell viability was measured. A middle cerebral artery occlusion followed by reperfusion model was used in vivo. Neurological function, encephalisation quotient, oedema, and volume of the cerebral infarction were then evaluated. The effects of piceatannol on histopathological findings, as well as the ultrastructure of the cortex, were analysed. The activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and lactate dehydrogenase (LDH) and the malondialdehyde (MDA) content was measured both in vitro and in vivo. Finally, the expression of nuclear factor erythroid-2-related factor 2 (Nrf2), hemeoxygenase-1 (HO-1), and nicotinamide adenine dinucleotide phosphate quinone oxidoreductase 1 (NQO1) in cerebral tissue was detected using reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blotting. Our results demonstrated that cell viability in the piceatannol groups was increased. The SOD, GSH-Px activities were increased as LDH activity and MDA content decreased in the piceatannol groups both in vitro and in vivo, reflecting a decrease in oxidative stress. The neurological severity score and infarction volume in the piceatannol groups at doses of 10 and 20 mg/kg were lower than those of the model group. Furthermore, the damage seen on histopathological examination was partially attenuated by piceatannol. RT-qPCR and western blot analysis indicated that the expression of Nrf2, HO-1, and NQO1 were significantly increased by piceatannol. The results of the study demonstrate that piceatannol exerts a protective effect against CIRI.</description><identifier>ISSN: 0364-3190</identifier><identifier>EISSN: 1573-6903</identifier><identifier>DOI: 10.1007/s11064-021-03328-8</identifier><identifier>PMID: 34031841</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Adenine ; Animals ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Brain - pathology ; Cardiovascular diseases ; Cell Biology ; Cell Hypoxia - physiology ; Cell Survival - drug effects ; Cell viability ; Cerebral blood flow ; Cerebral infarction ; Deprivation ; Edema ; Glucose - deficiency ; Glutathione ; Glutathione peroxidase ; Heme Oxygenase-1 - metabolism ; Infarction ; Infarction, Middle Cerebral Artery - drug therapy ; Infarction, Middle Cerebral Artery - metabolism ; Infarction, Middle Cerebral Artery - pathology ; Ischemia ; L-Lactate dehydrogenase ; Lactate dehydrogenase ; Lactic acid ; Male ; Malondialdehyde ; Membrane Proteins - metabolism ; Mice ; Mice, Inbred ICR ; NADPH-diaphorase ; Neurochemistry ; Neurology ; Neuroprotective Agents - therapeutic use ; Neurosciences ; NF-E2-Related Factor 2 - metabolism ; Nicotinamide ; Nicotinamide adenine dinucleotide ; Occlusion ; Original Paper ; Oxidative stress ; Oxidative Stress - drug effects ; Oxygen - metabolism ; Peroxidase ; Piceatannol ; Plants ; Polymerase chain reaction ; Quinone oxidoreductase ; Quinones ; Quotients ; Reperfusion ; Reperfusion Injury - drug therapy ; Reperfusion Injury - metabolism ; Reperfusion Injury - pathology ; Reverse transcription ; Signal Transduction - drug effects ; Stilbenes - therapeutic use ; Superoxide dismutase ; Ultrastructure ; Western blotting</subject><ispartof>Neurochemical research, 2021-07, Vol.46 (7), p.1869-1880</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021</rights><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-c62dce398abe4e44fac5791e9d7dfcf20dc57b81fcde6fc0fdc16e2a53ad6c9a3</citedby><cites>FETCH-LOGICAL-c375t-c62dce398abe4e44fac5791e9d7dfcf20dc57b81fcde6fc0fdc16e2a53ad6c9a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11064-021-03328-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11064-021-03328-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34031841$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Lingfeng</creatorcontrib><creatorcontrib>Guo, Ying</creatorcontrib><creatorcontrib>Ye, Jiayi</creatorcontrib><creatorcontrib>Pan, Zeyue</creatorcontrib><creatorcontrib>Hu, Peihao</creatorcontrib><creatorcontrib>Zhong, Xiaoming</creatorcontrib><creatorcontrib>Qiu, Fengmei</creatorcontrib><creatorcontrib>Zhang, Danni</creatorcontrib><creatorcontrib>Huang, Zhen</creatorcontrib><title>Protective Effect of Piceatannol Against Cerebral Ischaemia–Reperfusion Injury Via Regulating Nrf2/HO-1 Pathway In Vivo and Vitro</title><title>Neurochemical research</title><addtitle>Neurochem Res</addtitle><addtitle>Neurochem Res</addtitle><description>Piceatannol is a natural plant-derived compound with protective effects against cardiovascular diseases. However, its effect on cerebral ischaemia–reperfusion injury (CIRI) induced by oxidative stress remains unclear. This study aimed to investigate piceatannol’s antioxidation in CIRI. An in vitro oxygen–glucose deprivation followed by reoxygenation model was used and cell viability was measured. A middle cerebral artery occlusion followed by reperfusion model was used in vivo. Neurological function, encephalisation quotient, oedema, and volume of the cerebral infarction were then evaluated. The effects of piceatannol on histopathological findings, as well as the ultrastructure of the cortex, were analysed. The activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and lactate dehydrogenase (LDH) and the malondialdehyde (MDA) content was measured both in vitro and in vivo. Finally, the expression of nuclear factor erythroid-2-related factor 2 (Nrf2), hemeoxygenase-1 (HO-1), and nicotinamide adenine dinucleotide phosphate quinone oxidoreductase 1 (NQO1) in cerebral tissue was detected using reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blotting. Our results demonstrated that cell viability in the piceatannol groups was increased. The SOD, GSH-Px activities were increased as LDH activity and MDA content decreased in the piceatannol groups both in vitro and in vivo, reflecting a decrease in oxidative stress. The neurological severity score and infarction volume in the piceatannol groups at doses of 10 and 20 mg/kg were lower than those of the model group. Furthermore, the damage seen on histopathological examination was partially attenuated by piceatannol. RT-qPCR and western blot analysis indicated that the expression of Nrf2, HO-1, and NQO1 were significantly increased by piceatannol. The results of the study demonstrate that piceatannol exerts a protective effect against CIRI.</description><subject>Adenine</subject><subject>Animals</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain - pathology</subject><subject>Cardiovascular diseases</subject><subject>Cell Biology</subject><subject>Cell Hypoxia - physiology</subject><subject>Cell Survival - drug effects</subject><subject>Cell viability</subject><subject>Cerebral blood flow</subject><subject>Cerebral infarction</subject><subject>Deprivation</subject><subject>Edema</subject><subject>Glucose - deficiency</subject><subject>Glutathione</subject><subject>Glutathione peroxidase</subject><subject>Heme Oxygenase-1 - metabolism</subject><subject>Infarction</subject><subject>Infarction, Middle Cerebral Artery - drug therapy</subject><subject>Infarction, Middle Cerebral Artery - metabolism</subject><subject>Infarction, Middle Cerebral Artery - pathology</subject><subject>Ischemia</subject><subject>L-Lactate dehydrogenase</subject><subject>Lactate dehydrogenase</subject><subject>Lactic acid</subject><subject>Male</subject><subject>Malondialdehyde</subject><subject>Membrane Proteins - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred ICR</subject><subject>NADPH-diaphorase</subject><subject>Neurochemistry</subject><subject>Neurology</subject><subject>Neuroprotective Agents - therapeutic use</subject><subject>Neurosciences</subject><subject>NF-E2-Related Factor 2 - metabolism</subject><subject>Nicotinamide</subject><subject>Nicotinamide adenine dinucleotide</subject><subject>Occlusion</subject><subject>Original Paper</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Oxygen - metabolism</subject><subject>Peroxidase</subject><subject>Piceatannol</subject><subject>Plants</subject><subject>Polymerase chain reaction</subject><subject>Quinone oxidoreductase</subject><subject>Quinones</subject><subject>Quotients</subject><subject>Reperfusion</subject><subject>Reperfusion Injury - drug therapy</subject><subject>Reperfusion Injury - metabolism</subject><subject>Reperfusion Injury - pathology</subject><subject>Reverse transcription</subject><subject>Signal Transduction - drug effects</subject><subject>Stilbenes - therapeutic use</subject><subject>Superoxide dismutase</subject><subject>Ultrastructure</subject><subject>Western blotting</subject><issn>0364-3190</issn><issn>1573-6903</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kc1uUzEQhS0EoiHwAiyQJTZsLvXP_fFdVlGhkSoaVcDWmtjj9EY3drB9W2WHxCPwhjwJLikgsWDlseY7Z0ZzCHnJ2VvOWHeaOGdtXTHBKyalUJV6RGa86WTV9kw-JjMmS1vynp2QZyltGSsywZ-SE1kzyVXNZ-TbKoaMJg-3SM-dKxUNjq4Gg5DB-zDSsw0MPmW6wIjrCCNdJnMDuBvgx9fv17jH6KY0BE-XfjvFA_08AL3GzTRCHvyGfohOnF5cVZyuIN_cwaFwhbkNFLwtRY7hOXniYEz44uGdk0_vzj8uLqrLq_fLxdllZWTX5Mq0whqUvYI11ljXDkzT9Rx721lnnGC2_NeKO2OxdYY5a3iLAhoJtjU9yDl5c_Tdx_BlwpT1bkgGxxE8hilp0UghatWW48zJ63_QbZiiL9vdU0p1fS1locSRMjGkFNHpfRx2EA-aM30fkT5GpMvV9a-ItCqiVw_W03qH9o_kdyYFkEcglZbfYPw7-z-2PwEJ855_</recordid><startdate>20210701</startdate><enddate>20210701</enddate><creator>Wang, Lingfeng</creator><creator>Guo, Ying</creator><creator>Ye, Jiayi</creator><creator>Pan, Zeyue</creator><creator>Hu, Peihao</creator><creator>Zhong, Xiaoming</creator><creator>Qiu, Fengmei</creator><creator>Zhang, Danni</creator><creator>Huang, Zhen</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20210701</creationdate><title>Protective Effect of Piceatannol Against Cerebral Ischaemia–Reperfusion Injury Via Regulating Nrf2/HO-1 Pathway In Vivo and Vitro</title><author>Wang, Lingfeng ; Guo, Ying ; Ye, Jiayi ; Pan, Zeyue ; Hu, Peihao ; Zhong, Xiaoming ; Qiu, Fengmei ; Zhang, Danni ; Huang, Zhen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-c62dce398abe4e44fac5791e9d7dfcf20dc57b81fcde6fc0fdc16e2a53ad6c9a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Adenine</topic><topic>Animals</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Brain - pathology</topic><topic>Cardiovascular diseases</topic><topic>Cell Biology</topic><topic>Cell Hypoxia - physiology</topic><topic>Cell Survival - drug effects</topic><topic>Cell viability</topic><topic>Cerebral blood flow</topic><topic>Cerebral infarction</topic><topic>Deprivation</topic><topic>Edema</topic><topic>Glucose - deficiency</topic><topic>Glutathione</topic><topic>Glutathione peroxidase</topic><topic>Heme Oxygenase-1 - metabolism</topic><topic>Infarction</topic><topic>Infarction, Middle Cerebral Artery - drug therapy</topic><topic>Infarction, Middle Cerebral Artery - metabolism</topic><topic>Infarction, Middle Cerebral Artery - pathology</topic><topic>Ischemia</topic><topic>L-Lactate dehydrogenase</topic><topic>Lactate dehydrogenase</topic><topic>Lactic acid</topic><topic>Male</topic><topic>Malondialdehyde</topic><topic>Membrane Proteins - metabolism</topic><topic>Mice</topic><topic>Mice, Inbred ICR</topic><topic>NADPH-diaphorase</topic><topic>Neurochemistry</topic><topic>Neurology</topic><topic>Neuroprotective Agents - 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Academic</collection><jtitle>Neurochemical research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Lingfeng</au><au>Guo, Ying</au><au>Ye, Jiayi</au><au>Pan, Zeyue</au><au>Hu, Peihao</au><au>Zhong, Xiaoming</au><au>Qiu, Fengmei</au><au>Zhang, Danni</au><au>Huang, Zhen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Protective Effect of Piceatannol Against Cerebral Ischaemia–Reperfusion Injury Via Regulating Nrf2/HO-1 Pathway In Vivo and Vitro</atitle><jtitle>Neurochemical research</jtitle><stitle>Neurochem Res</stitle><addtitle>Neurochem Res</addtitle><date>2021-07-01</date><risdate>2021</risdate><volume>46</volume><issue>7</issue><spage>1869</spage><epage>1880</epage><pages>1869-1880</pages><issn>0364-3190</issn><eissn>1573-6903</eissn><abstract>Piceatannol is a natural plant-derived compound with protective effects against cardiovascular diseases. However, its effect on cerebral ischaemia–reperfusion injury (CIRI) induced by oxidative stress remains unclear. This study aimed to investigate piceatannol’s antioxidation in CIRI. An in vitro oxygen–glucose deprivation followed by reoxygenation model was used and cell viability was measured. A middle cerebral artery occlusion followed by reperfusion model was used in vivo. Neurological function, encephalisation quotient, oedema, and volume of the cerebral infarction were then evaluated. The effects of piceatannol on histopathological findings, as well as the ultrastructure of the cortex, were analysed. The activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and lactate dehydrogenase (LDH) and the malondialdehyde (MDA) content was measured both in vitro and in vivo. Finally, the expression of nuclear factor erythroid-2-related factor 2 (Nrf2), hemeoxygenase-1 (HO-1), and nicotinamide adenine dinucleotide phosphate quinone oxidoreductase 1 (NQO1) in cerebral tissue was detected using reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blotting. Our results demonstrated that cell viability in the piceatannol groups was increased. The SOD, GSH-Px activities were increased as LDH activity and MDA content decreased in the piceatannol groups both in vitro and in vivo, reflecting a decrease in oxidative stress. The neurological severity score and infarction volume in the piceatannol groups at doses of 10 and 20 mg/kg were lower than those of the model group. Furthermore, the damage seen on histopathological examination was partially attenuated by piceatannol. RT-qPCR and western blot analysis indicated that the expression of Nrf2, HO-1, and NQO1 were significantly increased by piceatannol. The results of the study demonstrate that piceatannol exerts a protective effect against CIRI.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>34031841</pmid><doi>10.1007/s11064-021-03328-8</doi><tpages>12</tpages></addata></record> |
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| ispartof | Neurochemical research, 2021-07, Vol.46 (7), p.1869-1880 |
| issn | 0364-3190 1573-6903 |
| language | eng |
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| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Adenine Animals Biochemistry Biomedical and Life Sciences Biomedicine Brain - pathology Cardiovascular diseases Cell Biology Cell Hypoxia - physiology Cell Survival - drug effects Cell viability Cerebral blood flow Cerebral infarction Deprivation Edema Glucose - deficiency Glutathione Glutathione peroxidase Heme Oxygenase-1 - metabolism Infarction Infarction, Middle Cerebral Artery - drug therapy Infarction, Middle Cerebral Artery - metabolism Infarction, Middle Cerebral Artery - pathology Ischemia L-Lactate dehydrogenase Lactate dehydrogenase Lactic acid Male Malondialdehyde Membrane Proteins - metabolism Mice Mice, Inbred ICR NADPH-diaphorase Neurochemistry Neurology Neuroprotective Agents - therapeutic use Neurosciences NF-E2-Related Factor 2 - metabolism Nicotinamide Nicotinamide adenine dinucleotide Occlusion Original Paper Oxidative stress Oxidative Stress - drug effects Oxygen - metabolism Peroxidase Piceatannol Plants Polymerase chain reaction Quinone oxidoreductase Quinones Quotients Reperfusion Reperfusion Injury - drug therapy Reperfusion Injury - metabolism Reperfusion Injury - pathology Reverse transcription Signal Transduction - drug effects Stilbenes - therapeutic use Superoxide dismutase Ultrastructure Western blotting |
| title | Protective Effect of Piceatannol Against Cerebral Ischaemia–Reperfusion Injury Via Regulating Nrf2/HO-1 Pathway In Vivo and Vitro |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-21T07%3A15%3A11IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Protective%20Effect%20of%20Piceatannol%20Against%20Cerebral%20Ischaemia%E2%80%93Reperfusion%20Injury%20Via%20Regulating%20Nrf2/HO-1%20Pathway%20In%20Vivo%20and%20Vitro&rft.jtitle=Neurochemical%20research&rft.au=Wang,%20Lingfeng&rft.date=2021-07-01&rft.volume=46&rft.issue=7&rft.spage=1869&rft.epage=1880&rft.pages=1869-1880&rft.issn=0364-3190&rft.eissn=1573-6903&rft_id=info:doi/10.1007/s11064-021-03328-8&rft_dat=%3Cproquest_cross%3E2532248640%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2538879433&rft_id=info:pmid/34031841&rfr_iscdi=true |