A New Approach for Exploring Reperfusion Brain Damage in Hypoxic Ischemic Encephalopathy
Reperfusion is an essential pathological stage in hypoxic ischemic encephalopathy (HIE). Although the Rice-Vannucci model is widely used in HIE research, it remains difficult to replicate HIE-related reperfusion brain injury. The purpose of this study is to establish a rat model of hypoxia ischemia...
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| Veröffentlicht in: | Molecular neurobiology 2024-03, Vol.61 (3), p.1417-1432 |
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| creator | Zhang, Tianlei Zhang, Zhiwei Geng, Jiayi Lin, Kexin Lin, Xinru Jiao, Mengdie Zhu, Jianghu Guo, Xiaoling Lin, Zhenlang |
| description | Reperfusion is an essential pathological stage in hypoxic ischemic encephalopathy (HIE). Although the Rice-Vannucci model is widely used in HIE research, it remains difficult to replicate HIE-related reperfusion brain injury. The purpose of this study is to establish a rat model of hypoxia ischemia reperfusion brain damage (HIRBD) using a common carotid artery (CCA) muscle bridge in order to investigate the mechanisms of cerebral resistance to hypoxic-ischemic and reperfusion brain damage. Random assignment of Sprague–Dawley (SD) rats to the Sham, HIRBD, and Rice-Vannucci groups. Changes in body weight, mortality rate, spontaneous alternation behavior test (SAB test), and dynamic changes in cerebral blood flow (CBF) were detected. The damaged cerebral cortices were extracted for morphological comparison, transcriptomic analysis, and quantitative real-time PCR. Harvesting the hippocampus for transmission electron microscopy (TEM) detection. As a result, CCA muscle bridge could effectively block CBF, which recovered after the muscle bridge detachment. Pathological comparison, the SAB test, and TEM analysis revealed that brain damage in Rice-Vannucci was more severe than HIRBD.
Gpx1, S100a6, Cldn5, Esr1,
and
Gfap
were highly expressed in both HIRBD and Rice-Vannucci. In conclusion, the CCA muscle bridge-established HIRBD model could be used as an innovative and dependable model to simulate pathological process of HIRBD.
Graphical Abstract |
| doi_str_mv | 10.1007/s12035-023-03645-9 |
| format | Article |
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Gpx1, S100a6, Cldn5, Esr1,
and
Gfap
were highly expressed in both HIRBD and Rice-Vannucci. In conclusion, the CCA muscle bridge-established HIRBD model could be used as an innovative and dependable model to simulate pathological process of HIRBD.
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Gpx1, S100a6, Cldn5, Esr1,
and
Gfap
were highly expressed in both HIRBD and Rice-Vannucci. In conclusion, the CCA muscle bridge-established HIRBD model could be used as an innovative and dependable model to simulate pathological process of HIRBD.
Graphical Abstract</description><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Blood flow</subject><subject>Body weight</subject><subject>Brain damage</subject><subject>Brain injury</subject><subject>Carotid artery</subject><subject>Cell Biology</subject><subject>Cerebral blood flow</subject><subject>Encephalopathy</subject><subject>ESR1 protein</subject><subject>Hypoxia</subject><subject>Ischemia</subject><subject>Neurobiology</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Reperfusion</subject><subject>Rice</subject><subject>Spontaneous alternation</subject><subject>Transcriptomics</subject><subject>Transmission electron microscopy</subject><issn>0893-7648</issn><issn>1559-1182</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><recordid>eNp9kMFuFDEMhiMEokvpC3BAkbhwGZo4mSRzXMpCK1UgoSL1FmVTpzvVzCQkO6L79qTd0ko9cLIPn3_bHyHvOPvEGdPHhQMTbcNANEwo2TbdC7Lgbds1nBt4SRbMdKLRSpoD8qaUG8YAONOvyYHQGrgyZkEul_Q7_qHLlHJ0fkNDzHR1m4aY--ma_sSEOcyljxP9nF0_0S9udNdIa3e6S_G29_Ss-A2OtVlNHtPGDTG57Wb3lrwKbih49FAPya-vq4uT0-b8x7ezk-V54wWobeMYBhHQa5AsaNeCNAwQRKcCMu-MlF76tRRGX_E1q2c7B5rrtWqlCQa0OCQf97n1gd8zlq0d--JxGNyEcS4WjFKcAxdtRT88Q2_inKd6nYVOcKMkb0WlYE_5HEvJGGzK_ejyznJm77zbvXdbvdt777arQ-8fouf1iFePI_9EV0DsgZLuzGJ-2v2f2L_qLowm</recordid><startdate>20240301</startdate><enddate>20240301</enddate><creator>Zhang, Tianlei</creator><creator>Zhang, Zhiwei</creator><creator>Geng, Jiayi</creator><creator>Lin, Kexin</creator><creator>Lin, Xinru</creator><creator>Jiao, Mengdie</creator><creator>Zhu, Jianghu</creator><creator>Guo, Xiaoling</creator><creator>Lin, Zhenlang</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QR</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-6850-0018</orcidid></search><sort><creationdate>20240301</creationdate><title>A New Approach for Exploring Reperfusion Brain Damage in Hypoxic Ischemic Encephalopathy</title><author>Zhang, Tianlei ; Zhang, Zhiwei ; Geng, Jiayi ; Lin, Kexin ; Lin, Xinru ; Jiao, Mengdie ; Zhu, Jianghu ; Guo, Xiaoling ; Lin, Zhenlang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c326t-a0ef3fec7240f7a524802e2396fe0ca844c4cb4387d1b0772aa2717b6548f8273</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Blood flow</topic><topic>Body weight</topic><topic>Brain damage</topic><topic>Brain injury</topic><topic>Carotid artery</topic><topic>Cell Biology</topic><topic>Cerebral blood flow</topic><topic>Encephalopathy</topic><topic>ESR1 protein</topic><topic>Hypoxia</topic><topic>Ischemia</topic><topic>Neurobiology</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>Reperfusion</topic><topic>Rice</topic><topic>Spontaneous alternation</topic><topic>Transcriptomics</topic><topic>Transmission electron microscopy</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Tianlei</creatorcontrib><creatorcontrib>Zhang, Zhiwei</creatorcontrib><creatorcontrib>Geng, Jiayi</creatorcontrib><creatorcontrib>Lin, Kexin</creatorcontrib><creatorcontrib>Lin, Xinru</creatorcontrib><creatorcontrib>Jiao, Mengdie</creatorcontrib><creatorcontrib>Zhu, Jianghu</creatorcontrib><creatorcontrib>Guo, Xiaoling</creatorcontrib><creatorcontrib>Lin, Zhenlang</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular neurobiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Tianlei</au><au>Zhang, Zhiwei</au><au>Geng, Jiayi</au><au>Lin, Kexin</au><au>Lin, Xinru</au><au>Jiao, Mengdie</au><au>Zhu, Jianghu</au><au>Guo, Xiaoling</au><au>Lin, Zhenlang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A New Approach for Exploring Reperfusion Brain Damage in Hypoxic Ischemic Encephalopathy</atitle><jtitle>Molecular neurobiology</jtitle><stitle>Mol Neurobiol</stitle><addtitle>Mol Neurobiol</addtitle><date>2024-03-01</date><risdate>2024</risdate><volume>61</volume><issue>3</issue><spage>1417</spage><epage>1432</epage><pages>1417-1432</pages><issn>0893-7648</issn><eissn>1559-1182</eissn><abstract>Reperfusion is an essential pathological stage in hypoxic ischemic encephalopathy (HIE). Although the Rice-Vannucci model is widely used in HIE research, it remains difficult to replicate HIE-related reperfusion brain injury. The purpose of this study is to establish a rat model of hypoxia ischemia reperfusion brain damage (HIRBD) using a common carotid artery (CCA) muscle bridge in order to investigate the mechanisms of cerebral resistance to hypoxic-ischemic and reperfusion brain damage. Random assignment of Sprague–Dawley (SD) rats to the Sham, HIRBD, and Rice-Vannucci groups. Changes in body weight, mortality rate, spontaneous alternation behavior test (SAB test), and dynamic changes in cerebral blood flow (CBF) were detected. The damaged cerebral cortices were extracted for morphological comparison, transcriptomic analysis, and quantitative real-time PCR. Harvesting the hippocampus for transmission electron microscopy (TEM) detection. As a result, CCA muscle bridge could effectively block CBF, which recovered after the muscle bridge detachment. Pathological comparison, the SAB test, and TEM analysis revealed that brain damage in Rice-Vannucci was more severe than HIRBD.
Gpx1, S100a6, Cldn5, Esr1,
and
Gfap
were highly expressed in both HIRBD and Rice-Vannucci. In conclusion, the CCA muscle bridge-established HIRBD model could be used as an innovative and dependable model to simulate pathological process of HIRBD.
Graphical Abstract</abstract><cop>New York</cop><pub>Springer US</pub><pmid>37721688</pmid><doi>10.1007/s12035-023-03645-9</doi><tpages>16</tpages><orcidid>https://orcid.org/0000-0001-6850-0018</orcidid></addata></record> |
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| subjects | Biomedical and Life Sciences Biomedicine Blood flow Body weight Brain damage Brain injury Carotid artery Cell Biology Cerebral blood flow Encephalopathy ESR1 protein Hypoxia Ischemia Neurobiology Neurology Neurosciences Reperfusion Rice Spontaneous alternation Transcriptomics Transmission electron microscopy |
| title | A New Approach for Exploring Reperfusion Brain Damage in Hypoxic Ischemic Encephalopathy |
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