Oridonin prevents oxidative stress‐induced endothelial injury via promoting Nrf‐2 pathway in ischaemic stroke
Oridonin, a natural diterpenoid compound extracted from a Chinese herb, has been proved to exert anti‐oxidative stress effects in various disease models. The aim of the present study was to investigate the protective effects of oridonin on oxidative stress‐induced endothelial injury in ischaemic str...
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| Veröffentlicht in: | Journal of cellular and molecular medicine 2021-10, Vol.25 (20), p.9753-9766 |
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| creator | Li, Lei Cheng, Shu‐Qi Guo, Wei Cai, Zhen‐Yu Sun, Yu‐Qin Huang, Xin‐Xin Yang, Jin Ji, Juan Chen, Ya‐Yun Dong, Yin‐Feng Cheng, Hong Sun, Xiu‐Lan |
| description | Oridonin, a natural diterpenoid compound extracted from a Chinese herb, has been proved to exert anti‐oxidative stress effects in various disease models. The aim of the present study was to investigate the protective effects of oridonin on oxidative stress‐induced endothelial injury in ischaemic stroke. We found oridonin repaired blood‐brain barrier (BBB) integrity presented with upregulation of tight junction proteins (TJ proteins) expression, inhibited the infiltration of periphery inflammatory cells and neuroinflammation and thereby reduced infarct volume in ischaemic stroke mice. Furthermore, our results showed that oridonin could protect against oxidative stress‐induced endothelial injury via promoting nuclear translocation of nuclear factor‐erythroid 2 related factor 2 (Nrf‐2). The specific mechanism could be the activation of AKT(Ser473)/GSK3β(Ser9)/Fyn signalling pathway. Our findings revealed the therapeutic effect and mechanism of oridonin in ischaemic stroke, which provided fundamental evidence for developing the extracted compound of Chinese herbal medicine into an innovative drug for ischaemic stroke treatment. |
| doi_str_mv | 10.1111/jcmm.16923 |
| format | Article |
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The aim of the present study was to investigate the protective effects of oridonin on oxidative stress‐induced endothelial injury in ischaemic stroke. We found oridonin repaired blood‐brain barrier (BBB) integrity presented with upregulation of tight junction proteins (TJ proteins) expression, inhibited the infiltration of periphery inflammatory cells and neuroinflammation and thereby reduced infarct volume in ischaemic stroke mice. Furthermore, our results showed that oridonin could protect against oxidative stress‐induced endothelial injury via promoting nuclear translocation of nuclear factor‐erythroid 2 related factor 2 (Nrf‐2). The specific mechanism could be the activation of AKT(Ser473)/GSK3β(Ser9)/Fyn signalling pathway. Our findings revealed the therapeutic effect and mechanism of oridonin in ischaemic stroke, which provided fundamental evidence for developing the extracted compound of Chinese herbal medicine into an innovative drug for ischaemic stroke treatment.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.16923</identifier><identifier>PMID: 34514714</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>AKT protein ; Animal welfare ; Animals ; Anti-Inflammatory Agents - pharmacology ; Antibodies ; Biomarkers ; Blood-brain barrier ; Blood-Brain Barrier - metabolism ; Brain ; Capillary Permeability ; Carotid arteries ; Cell Survival - drug effects ; Disease Models, Animal ; Disease Susceptibility ; Diterpenes ; Diterpenes, Kaurane - pharmacology ; endothelial cell ; Endothelium - drug effects ; Endothelium - metabolism ; Endothelium - pathology ; Experiments ; Fyn protein ; Glucose - metabolism ; Glycogen Synthase Kinase 3 beta - metabolism ; Herbal medicine ; Immunohistochemistry ; Inflammation ; Injuries ; ischaemic stroke ; Ischemia ; Ischemic Stroke - etiology ; Ischemic Stroke - metabolism ; Male ; Medical research ; Mice ; Neurons - drug effects ; Neurons - metabolism ; NF-E2-Related Factor 2 - metabolism ; Nrf‐2 ; Nuclear transport ; oridonin ; Original ; Oxidative stress ; Oxidative Stress - drug effects ; Oxygen - metabolism ; Permeability ; Proto-Oncogene Proteins c-akt - metabolism ; Reactive Oxygen Species - metabolism ; Signal transduction ; Signal Transduction - drug effects ; Stroke ; Veins & arteries</subject><ispartof>Journal of cellular and molecular medicine, 2021-10, Vol.25 (20), p.9753-9766</ispartof><rights>2021 The Authors. published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2021 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2021. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4483-9105e50a0083bab051d0a1626f3155f8485abbfdbed304b9736482a194e644173</citedby><cites>FETCH-LOGICAL-c4483-9105e50a0083bab051d0a1626f3155f8485abbfdbed304b9736482a194e644173</cites><orcidid>0000-0001-8741-3833</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8505855/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8505855/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,1417,11562,27924,27925,45574,45575,46052,46476,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34514714$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Lei</creatorcontrib><creatorcontrib>Cheng, Shu‐Qi</creatorcontrib><creatorcontrib>Guo, Wei</creatorcontrib><creatorcontrib>Cai, Zhen‐Yu</creatorcontrib><creatorcontrib>Sun, Yu‐Qin</creatorcontrib><creatorcontrib>Huang, Xin‐Xin</creatorcontrib><creatorcontrib>Yang, Jin</creatorcontrib><creatorcontrib>Ji, Juan</creatorcontrib><creatorcontrib>Chen, Ya‐Yun</creatorcontrib><creatorcontrib>Dong, Yin‐Feng</creatorcontrib><creatorcontrib>Cheng, Hong</creatorcontrib><creatorcontrib>Sun, Xiu‐Lan</creatorcontrib><title>Oridonin prevents oxidative stress‐induced endothelial injury via promoting Nrf‐2 pathway in ischaemic stroke</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>Oridonin, a natural diterpenoid compound extracted from a Chinese herb, has been proved to exert anti‐oxidative stress effects in various disease models. The aim of the present study was to investigate the protective effects of oridonin on oxidative stress‐induced endothelial injury in ischaemic stroke. We found oridonin repaired blood‐brain barrier (BBB) integrity presented with upregulation of tight junction proteins (TJ proteins) expression, inhibited the infiltration of periphery inflammatory cells and neuroinflammation and thereby reduced infarct volume in ischaemic stroke mice. Furthermore, our results showed that oridonin could protect against oxidative stress‐induced endothelial injury via promoting nuclear translocation of nuclear factor‐erythroid 2 related factor 2 (Nrf‐2). The specific mechanism could be the activation of AKT(Ser473)/GSK3β(Ser9)/Fyn signalling pathway. Our findings revealed the therapeutic effect and mechanism of oridonin in ischaemic stroke, which provided fundamental evidence for developing the extracted compound of Chinese herbal medicine into an innovative drug for ischaemic stroke treatment.</description><subject>AKT protein</subject><subject>Animal welfare</subject><subject>Animals</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Antibodies</subject><subject>Biomarkers</subject><subject>Blood-brain barrier</subject><subject>Blood-Brain Barrier - metabolism</subject><subject>Brain</subject><subject>Capillary Permeability</subject><subject>Carotid arteries</subject><subject>Cell Survival - drug effects</subject><subject>Disease Models, Animal</subject><subject>Disease Susceptibility</subject><subject>Diterpenes</subject><subject>Diterpenes, Kaurane - pharmacology</subject><subject>endothelial cell</subject><subject>Endothelium - drug effects</subject><subject>Endothelium - metabolism</subject><subject>Endothelium - pathology</subject><subject>Experiments</subject><subject>Fyn protein</subject><subject>Glucose - metabolism</subject><subject>Glycogen Synthase Kinase 3 beta - metabolism</subject><subject>Herbal medicine</subject><subject>Immunohistochemistry</subject><subject>Inflammation</subject><subject>Injuries</subject><subject>ischaemic stroke</subject><subject>Ischemia</subject><subject>Ischemic Stroke - etiology</subject><subject>Ischemic Stroke - metabolism</subject><subject>Male</subject><subject>Medical research</subject><subject>Mice</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>NF-E2-Related Factor 2 - metabolism</subject><subject>Nrf‐2</subject><subject>Nuclear transport</subject><subject>oridonin</subject><subject>Original</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Oxygen - metabolism</subject><subject>Permeability</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Stroke</subject><subject>Veins & arteries</subject><issn>1582-1838</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><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>eNp9kc1uEzEURq0K1JbSTR-gssQGVUrxHdsTz6YSiig_aumGri3P-E7jMGOn9kxKdjwCz8iT4JBQQRd4Y0s-PrqfP0JOgJ1DXm8WTd-fQ1kVfI8cglTFRFRcPNudQXF1QF6ktGCMl8CrfXLAhQQxBXFI7m-is8E7T5cRV-iHRMM3Z83gVkjTEDGln99_OG_HBi1Fb8Mwx86Zjjq_GOOarpzJT0MfBufv6OfYZrygSzPMH8w6Q9SlZm6wd81GF77iS_K8NV3C491-RG4v332ZfZhc3bz_OHt7NWmEUHxSAZMomWFM8drUTIJlBsqibDlI2SqhpKnr1tZoORN1NeWlUIWBSmApBEz5EbnYepdj3aNtcrZoOr2MrjdxrYNx-t8b7-b6Lqy0kkwqKbPg9U4Qw_2IadB9zoJdZzyGMelCTosC8r-rjL56gi7CGH2OlymVE3BZskydbakmhpQito_DANObJvWmSf27yQyf_j3-I_qnugzAFnhwHa7_o9KfZtfXW-kvz8qs3w</recordid><startdate>202110</startdate><enddate>202110</enddate><creator>Li, Lei</creator><creator>Cheng, Shu‐Qi</creator><creator>Guo, Wei</creator><creator>Cai, Zhen‐Yu</creator><creator>Sun, Yu‐Qin</creator><creator>Huang, Xin‐Xin</creator><creator>Yang, Jin</creator><creator>Ji, Juan</creator><creator>Chen, Ya‐Yun</creator><creator>Dong, Yin‐Feng</creator><creator>Cheng, Hong</creator><creator>Sun, Xiu‐Lan</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</scope><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>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</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>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>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-8741-3833</orcidid></search><sort><creationdate>202110</creationdate><title>Oridonin prevents oxidative stress‐induced endothelial injury via promoting Nrf‐2 pathway in ischaemic stroke</title><author>Li, Lei ; Cheng, Shu‐Qi ; Guo, Wei ; Cai, Zhen‐Yu ; Sun, Yu‐Qin ; Huang, Xin‐Xin ; Yang, Jin ; Ji, Juan ; Chen, Ya‐Yun ; Dong, Yin‐Feng ; Cheng, Hong ; Sun, Xiu‐Lan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4483-9105e50a0083bab051d0a1626f3155f8485abbfdbed304b9736482a194e644173</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>AKT protein</topic><topic>Animal welfare</topic><topic>Animals</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Antibodies</topic><topic>Biomarkers</topic><topic>Blood-brain barrier</topic><topic>Blood-Brain Barrier - metabolism</topic><topic>Brain</topic><topic>Capillary Permeability</topic><topic>Carotid arteries</topic><topic>Cell Survival - drug effects</topic><topic>Disease Models, Animal</topic><topic>Disease Susceptibility</topic><topic>Diterpenes</topic><topic>Diterpenes, Kaurane - pharmacology</topic><topic>endothelial cell</topic><topic>Endothelium - drug effects</topic><topic>Endothelium - metabolism</topic><topic>Endothelium - pathology</topic><topic>Experiments</topic><topic>Fyn protein</topic><topic>Glucose - metabolism</topic><topic>Glycogen Synthase Kinase 3 beta - metabolism</topic><topic>Herbal medicine</topic><topic>Immunohistochemistry</topic><topic>Inflammation</topic><topic>Injuries</topic><topic>ischaemic stroke</topic><topic>Ischemia</topic><topic>Ischemic Stroke - etiology</topic><topic>Ischemic Stroke - metabolism</topic><topic>Male</topic><topic>Medical research</topic><topic>Mice</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>NF-E2-Related Factor 2 - metabolism</topic><topic>Nrf‐2</topic><topic>Nuclear transport</topic><topic>oridonin</topic><topic>Original</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Oxygen - metabolism</topic><topic>Permeability</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>Stroke</topic><topic>Veins & arteries</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Lei</creatorcontrib><creatorcontrib>Cheng, Shu‐Qi</creatorcontrib><creatorcontrib>Guo, Wei</creatorcontrib><creatorcontrib>Cai, Zhen‐Yu</creatorcontrib><creatorcontrib>Sun, Yu‐Qin</creatorcontrib><creatorcontrib>Huang, Xin‐Xin</creatorcontrib><creatorcontrib>Yang, Jin</creatorcontrib><creatorcontrib>Ji, Juan</creatorcontrib><creatorcontrib>Chen, Ya‐Yun</creatorcontrib><creatorcontrib>Dong, Yin‐Feng</creatorcontrib><creatorcontrib>Cheng, Hong</creatorcontrib><creatorcontrib>Sun, Xiu‐Lan</creatorcontrib><collection>Wiley Online Library</collection><collection>Wiley Online Library</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>ProQuest Health and Medical</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Science Journals</collection><collection>ProQuest Biological Science Journals</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Access via ProQuest (Open Access)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cellular and molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Lei</au><au>Cheng, Shu‐Qi</au><au>Guo, Wei</au><au>Cai, Zhen‐Yu</au><au>Sun, Yu‐Qin</au><au>Huang, Xin‐Xin</au><au>Yang, Jin</au><au>Ji, Juan</au><au>Chen, Ya‐Yun</au><au>Dong, Yin‐Feng</au><au>Cheng, Hong</au><au>Sun, Xiu‐Lan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oridonin prevents oxidative stress‐induced endothelial injury via promoting Nrf‐2 pathway in ischaemic stroke</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2021-10</date><risdate>2021</risdate><volume>25</volume><issue>20</issue><spage>9753</spage><epage>9766</epage><pages>9753-9766</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>Oridonin, a natural diterpenoid compound extracted from a Chinese herb, has been proved to exert anti‐oxidative stress effects in various disease models. The aim of the present study was to investigate the protective effects of oridonin on oxidative stress‐induced endothelial injury in ischaemic stroke. We found oridonin repaired blood‐brain barrier (BBB) integrity presented with upregulation of tight junction proteins (TJ proteins) expression, inhibited the infiltration of periphery inflammatory cells and neuroinflammation and thereby reduced infarct volume in ischaemic stroke mice. Furthermore, our results showed that oridonin could protect against oxidative stress‐induced endothelial injury via promoting nuclear translocation of nuclear factor‐erythroid 2 related factor 2 (Nrf‐2). The specific mechanism could be the activation of AKT(Ser473)/GSK3β(Ser9)/Fyn signalling pathway. Our findings revealed the therapeutic effect and mechanism of oridonin in ischaemic stroke, which provided fundamental evidence for developing the extracted compound of Chinese herbal medicine into an innovative drug for ischaemic stroke treatment.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>34514714</pmid><doi>10.1111/jcmm.16923</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0001-8741-3833</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | AKT protein Animal welfare Animals Anti-Inflammatory Agents - pharmacology Antibodies Biomarkers Blood-brain barrier Blood-Brain Barrier - metabolism Brain Capillary Permeability Carotid arteries Cell Survival - drug effects Disease Models, Animal Disease Susceptibility Diterpenes Diterpenes, Kaurane - pharmacology endothelial cell Endothelium - drug effects Endothelium - metabolism Endothelium - pathology Experiments Fyn protein Glucose - metabolism Glycogen Synthase Kinase 3 beta - metabolism Herbal medicine Immunohistochemistry Inflammation Injuries ischaemic stroke Ischemia Ischemic Stroke - etiology Ischemic Stroke - metabolism Male Medical research Mice Neurons - drug effects Neurons - metabolism NF-E2-Related Factor 2 - metabolism Nrf‐2 Nuclear transport oridonin Original Oxidative stress Oxidative Stress - drug effects Oxygen - metabolism Permeability Proto-Oncogene Proteins c-akt - metabolism Reactive Oxygen Species - metabolism Signal transduction Signal Transduction - drug effects Stroke Veins & arteries |
| title | Oridonin prevents oxidative stress‐induced endothelial injury via promoting Nrf‐2 pathway in ischaemic stroke |
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