Zinc Regulates Glucose Metabolism of the Spinal Cord and Neurons and Promotes Functional Recovery after Spinal Cord Injury through the AMPK Signaling Pathway
Spinal cord injury (SCI) is a traumatic disease that can cause severe nervous system dysfunction. SCI often causes spinal cord mitochondrial dysfunction and produces glucose metabolism disorders, which affect neuronal survival. Zinc is an essential trace element in the human body and plays multiple...
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| Veröffentlicht in: | Oxidative medicine and cellular longevity 2021, Vol.2021 (1), p.4331625-4331625 |
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| container_title | Oxidative medicine and cellular longevity |
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| creator | Hu, Hengshuo Xia, Nan Lin, Jiaquan Li, Daoyong Zhang, Chuanjie Ge, Minghao Tian, He Mei, Xifan |
| description | Spinal cord injury (SCI) is a traumatic disease that can cause severe nervous system dysfunction. SCI often causes spinal cord mitochondrial dysfunction and produces glucose metabolism disorders, which affect neuronal survival. Zinc is an essential trace element in the human body and plays multiple roles in the nervous system. This experiment is intended to evaluate whether zinc can regulate the spinal cord and neuronal glucose metabolism and promote motor functional recovery after SCI. Then we explore its molecular mechanism. We evaluated the function of zinc from the aspects of glucose uptake and the protection of the mitochondria in vivo and in vitro. The results showed that zinc elevated the expression level of GLUT4 and promoted glucose uptake. Zinc enhanced the expression of proteins such as PGC-1α and NRF2, reduced oxidative stress, and promoted mitochondrial production. In addition, zinc decreased neuronal apoptosis and promoted the recovery of motor function in SCI mice. After administration of AMPK inhibitor, the therapeutic effect of zinc was reversed. Therefore, we concluded that zinc regulated the glucose metabolism of the spinal cord and neurons and promoted functional recovery after SCI through the AMPK pathway, which is expected to become a potential treatment strategy for SCI. |
| doi_str_mv | 10.1155/2021/4331625 |
| format | Article |
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SCI often causes spinal cord mitochondrial dysfunction and produces glucose metabolism disorders, which affect neuronal survival. Zinc is an essential trace element in the human body and plays multiple roles in the nervous system. This experiment is intended to evaluate whether zinc can regulate the spinal cord and neuronal glucose metabolism and promote motor functional recovery after SCI. Then we explore its molecular mechanism. We evaluated the function of zinc from the aspects of glucose uptake and the protection of the mitochondria in vivo and in vitro. The results showed that zinc elevated the expression level of GLUT4 and promoted glucose uptake. Zinc enhanced the expression of proteins such as PGC-1α and NRF2, reduced oxidative stress, and promoted mitochondrial production. In addition, zinc decreased neuronal apoptosis and promoted the recovery of motor function in SCI mice. After administration of AMPK inhibitor, the therapeutic effect of zinc was reversed. Therefore, we concluded that zinc regulated the glucose metabolism of the spinal cord and neurons and promoted functional recovery after SCI through the AMPK pathway, which is expected to become a potential treatment strategy for SCI.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2021/4331625</identifier><identifier>PMID: 34373765</identifier><language>eng</language><publisher>United States: Hindawi</publisher><subject>Adenylate Kinase - metabolism ; Animals ; Apoptosis ; Contusions ; Female ; Glucose ; Glucose - metabolism ; Glucose Transporter Type 4 - metabolism ; Hypoxia ; Ischemia ; Kinases ; Male ; Metabolic disorders ; Mice ; Mice, Inbred C57BL ; Mitochondria ; Mitochondria - drug effects ; Mitochondria - metabolism ; Nervous system ; Neurons - drug effects ; Neurons - metabolism ; NF-E2-Related Factor 2 - metabolism ; Oxidative stress ; PC12 Cells ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism ; Rats ; Signal Transduction ; Spinal Cord - cytology ; Spinal Cord - metabolism ; Spinal Cord - physiology ; Spinal cord injuries ; Spinal Cord Injuries - drug therapy ; Spinal Cord Injuries - metabolism ; Spinal Cord Regeneration ; Zinc - pharmacology ; Zinc - therapeutic use</subject><ispartof>Oxidative medicine and cellular longevity, 2021, Vol.2021 (1), p.4331625-4331625</ispartof><rights>Copyright © 2021 Hengshuo Hu et al.</rights><rights>Copyright © 2021 Hengshuo Hu 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. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2021 Hengshuo Hu et al. 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c514t-6fb3ab862a3fb2905a25551e3961a036b4cc3629beac682a0e1d8571e52b7653</citedby><cites>FETCH-LOGICAL-c514t-6fb3ab862a3fb2905a25551e3961a036b4cc3629beac682a0e1d8571e52b7653</cites><orcidid>0000-0003-3698-0525 ; 0000-0001-8105-9773</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/PMC8349299/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8349299/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,4022,27922,27923,27924,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34373765$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Sita, Giulia</contributor><contributor>Giulia Sita</contributor><creatorcontrib>Hu, Hengshuo</creatorcontrib><creatorcontrib>Xia, Nan</creatorcontrib><creatorcontrib>Lin, Jiaquan</creatorcontrib><creatorcontrib>Li, Daoyong</creatorcontrib><creatorcontrib>Zhang, Chuanjie</creatorcontrib><creatorcontrib>Ge, Minghao</creatorcontrib><creatorcontrib>Tian, He</creatorcontrib><creatorcontrib>Mei, Xifan</creatorcontrib><title>Zinc Regulates Glucose Metabolism of the Spinal Cord and Neurons and Promotes Functional Recovery after Spinal Cord Injury through the AMPK Signaling Pathway</title><title>Oxidative medicine and cellular longevity</title><addtitle>Oxid Med Cell Longev</addtitle><description>Spinal cord injury (SCI) is a traumatic disease that can cause severe nervous system dysfunction. SCI often causes spinal cord mitochondrial dysfunction and produces glucose metabolism disorders, which affect neuronal survival. Zinc is an essential trace element in the human body and plays multiple roles in the nervous system. This experiment is intended to evaluate whether zinc can regulate the spinal cord and neuronal glucose metabolism and promote motor functional recovery after SCI. Then we explore its molecular mechanism. We evaluated the function of zinc from the aspects of glucose uptake and the protection of the mitochondria in vivo and in vitro. The results showed that zinc elevated the expression level of GLUT4 and promoted glucose uptake. Zinc enhanced the expression of proteins such as PGC-1α and NRF2, reduced oxidative stress, and promoted mitochondrial production. In addition, zinc decreased neuronal apoptosis and promoted the recovery of motor function in SCI mice. After administration of AMPK inhibitor, the therapeutic effect of zinc was reversed. Therefore, we concluded that zinc regulated the glucose metabolism of the spinal cord and neurons and promoted functional recovery after SCI through the AMPK pathway, which is expected to become a potential treatment strategy for SCI.</description><subject>Adenylate Kinase - metabolism</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Contusions</subject><subject>Female</subject><subject>Glucose</subject><subject>Glucose - metabolism</subject><subject>Glucose Transporter Type 4 - metabolism</subject><subject>Hypoxia</subject><subject>Ischemia</subject><subject>Kinases</subject><subject>Male</subject><subject>Metabolic disorders</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mitochondria</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - metabolism</subject><subject>Nervous system</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>NF-E2-Related Factor 2 - metabolism</subject><subject>Oxidative stress</subject><subject>PC12 Cells</subject><subject>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism</subject><subject>Rats</subject><subject>Signal Transduction</subject><subject>Spinal Cord - cytology</subject><subject>Spinal Cord - metabolism</subject><subject>Spinal Cord - physiology</subject><subject>Spinal cord injuries</subject><subject>Spinal Cord Injuries - drug therapy</subject><subject>Spinal Cord Injuries - metabolism</subject><subject>Spinal Cord Regeneration</subject><subject>Zinc - pharmacology</subject><subject>Zinc - therapeutic use</subject><issn>1942-0900</issn><issn>1942-0994</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp9kU1vEzEQhleIipbCjTOyxAUJQv2xduILUhXRUrWFqO2Ji-X1zu462tjBH63yY_iv7DYhohw4eaR55pFn3qJ4Q_AnQjg_oZiSk5IxIih_VhwRWdIJlrJ8vq8xPixexrjEWDBakhfFISvZlE0FPyp-_bDOoBtoc68TRHTeZ-MjoGtIuvK9jSvkG5Q6QLdr63SP5j7USLsafYMcvIuP9SL4lR_Hz7IzyfoRvAHj7yFskG4ShCfjF26Zh0bqgs9t92g_vV5colvbDox1LVro1D3ozavioNF9hNe797i4O_tyN_86ufp-fjE_vZoYTso0EU3FdDUTVLOmohJzTTnnBJgURGMmqtIYJqisQBsxoxoDqWd8SoDTargCOy4-b7XrXK2gNuBS0L1aB7vSYaO8tuppx9lOtf5ezVgpqZSD4P1OEPzPDDGplY0G-l478DkqygXGXAhBB_TdP-jS5zCsPVJcMiYpEwP1cUuZ4GMM0Ow_Q7AaY1dj7GoX-4C__XuBPfwn5wH4sAU662r9YP-v-w0CZLaI</recordid><startdate>2021</startdate><enddate>2021</enddate><creator>Hu, Hengshuo</creator><creator>Xia, Nan</creator><creator>Lin, Jiaquan</creator><creator>Li, Daoyong</creator><creator>Zhang, Chuanjie</creator><creator>Ge, Minghao</creator><creator>Tian, He</creator><creator>Mei, Xifan</creator><general>Hindawi</general><general>Hindawi Limited</general><scope>RHU</scope><scope>RHW</scope><scope>RHX</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-3698-0525</orcidid><orcidid>https://orcid.org/0000-0001-8105-9773</orcidid></search><sort><creationdate>2021</creationdate><title>Zinc Regulates Glucose Metabolism of the Spinal Cord and Neurons and Promotes Functional Recovery after Spinal Cord Injury through the AMPK Signaling Pathway</title><author>Hu, Hengshuo ; Xia, Nan ; Lin, Jiaquan ; Li, Daoyong ; Zhang, Chuanjie ; Ge, Minghao ; Tian, He ; Mei, Xifan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c514t-6fb3ab862a3fb2905a25551e3961a036b4cc3629beac682a0e1d8571e52b7653</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Adenylate Kinase - metabolism</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Contusions</topic><topic>Female</topic><topic>Glucose</topic><topic>Glucose - metabolism</topic><topic>Glucose Transporter Type 4 - metabolism</topic><topic>Hypoxia</topic><topic>Ischemia</topic><topic>Kinases</topic><topic>Male</topic><topic>Metabolic disorders</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mitochondria</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - metabolism</topic><topic>Nervous system</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>NF-E2-Related Factor 2 - metabolism</topic><topic>Oxidative stress</topic><topic>PC12 Cells</topic><topic>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism</topic><topic>Rats</topic><topic>Signal Transduction</topic><topic>Spinal Cord - cytology</topic><topic>Spinal Cord - metabolism</topic><topic>Spinal Cord - physiology</topic><topic>Spinal cord injuries</topic><topic>Spinal Cord Injuries - drug therapy</topic><topic>Spinal Cord Injuries - metabolism</topic><topic>Spinal Cord Regeneration</topic><topic>Zinc - pharmacology</topic><topic>Zinc - therapeutic use</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hu, Hengshuo</creatorcontrib><creatorcontrib>Xia, Nan</creatorcontrib><creatorcontrib>Lin, Jiaquan</creatorcontrib><creatorcontrib>Li, Daoyong</creatorcontrib><creatorcontrib>Zhang, Chuanjie</creatorcontrib><creatorcontrib>Ge, Minghao</creatorcontrib><creatorcontrib>Tian, He</creatorcontrib><creatorcontrib>Mei, Xifan</creatorcontrib><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access Journals</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oxidative medicine and cellular longevity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hu, Hengshuo</au><au>Xia, Nan</au><au>Lin, Jiaquan</au><au>Li, Daoyong</au><au>Zhang, Chuanjie</au><au>Ge, Minghao</au><au>Tian, He</au><au>Mei, Xifan</au><au>Sita, Giulia</au><au>Giulia Sita</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Zinc Regulates Glucose Metabolism of the Spinal Cord and Neurons and Promotes Functional Recovery after Spinal Cord Injury through the AMPK Signaling Pathway</atitle><jtitle>Oxidative medicine and cellular longevity</jtitle><addtitle>Oxid Med Cell Longev</addtitle><date>2021</date><risdate>2021</risdate><volume>2021</volume><issue>1</issue><spage>4331625</spage><epage>4331625</epage><pages>4331625-4331625</pages><issn>1942-0900</issn><eissn>1942-0994</eissn><abstract>Spinal cord injury (SCI) is a traumatic disease that can cause severe nervous system dysfunction. SCI often causes spinal cord mitochondrial dysfunction and produces glucose metabolism disorders, which affect neuronal survival. Zinc is an essential trace element in the human body and plays multiple roles in the nervous system. This experiment is intended to evaluate whether zinc can regulate the spinal cord and neuronal glucose metabolism and promote motor functional recovery after SCI. Then we explore its molecular mechanism. We evaluated the function of zinc from the aspects of glucose uptake and the protection of the mitochondria in vivo and in vitro. The results showed that zinc elevated the expression level of GLUT4 and promoted glucose uptake. Zinc enhanced the expression of proteins such as PGC-1α and NRF2, reduced oxidative stress, and promoted mitochondrial production. In addition, zinc decreased neuronal apoptosis and promoted the recovery of motor function in SCI mice. After administration of AMPK inhibitor, the therapeutic effect of zinc was reversed. Therefore, we concluded that zinc regulated the glucose metabolism of the spinal cord and neurons and promoted functional recovery after SCI through the AMPK pathway, which is expected to become a potential treatment strategy for SCI.</abstract><cop>United States</cop><pub>Hindawi</pub><pmid>34373765</pmid><doi>10.1155/2021/4331625</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0003-3698-0525</orcidid><orcidid>https://orcid.org/0000-0001-8105-9773</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Adenylate Kinase - metabolism Animals Apoptosis Contusions Female Glucose Glucose - metabolism Glucose Transporter Type 4 - metabolism Hypoxia Ischemia Kinases Male Metabolic disorders Mice Mice, Inbred C57BL Mitochondria Mitochondria - drug effects Mitochondria - metabolism Nervous system Neurons - drug effects Neurons - metabolism NF-E2-Related Factor 2 - metabolism Oxidative stress PC12 Cells Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism Rats Signal Transduction Spinal Cord - cytology Spinal Cord - metabolism Spinal Cord - physiology Spinal cord injuries Spinal Cord Injuries - drug therapy Spinal Cord Injuries - metabolism Spinal Cord Regeneration Zinc - pharmacology Zinc - therapeutic use |
| title | Zinc Regulates Glucose Metabolism of the Spinal Cord and Neurons and Promotes Functional Recovery after Spinal Cord Injury through the AMPK Signaling Pathway |
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