PPAR-alpha and PPAR-beta expression changes in the hippocampus of rats undergoing global cerebral ischemia/reperfusion due to PPAR-gamma status
Peroxisome proliferator-activated receptors (PPARs, including alpha, beta and gamma subtypes) and their agonists have a protective role in treatment of central nervous system (CNS) diseases. The present study was designed to investigate the expression changes of PPAR-alpha, -beta, -gamma and NF-kapp...
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description | Peroxisome proliferator-activated receptors (PPARs, including alpha, beta and gamma subtypes) and their agonists have a protective role in treatment of central nervous system (CNS) diseases. The present study was designed to investigate the expression changes of PPAR-alpha, -beta, -gamma and NF-kappa B in the hippocampus of rats with global cerebral ischemia/reperfusion injury (GCIRI) after treatment with agonists or antagonists of PPAR-gamma.
A rat GCIRI model was established by occlusion of bilateral common carotid arteries and cervical vena retransfusion. GW9662 (5 μg), a selective PPAR- gamma antagonist, was intraventricularly injected at 0.5 h before GCIR; Rosiglitazone (0.8, 2.4 and 7.2 mg/kg), a selective PPAR- gamma agonist, was injected intraperitoneally at 1 h before GCIRI. The expression changes of PPAR-alpha, -beta and -gamma at mRNA and protein levels were detected by RT-PCR and western blotting. The changes of spatial learning and memory (SLM) functions were assessed by using a Morris water maze; the pathohistological changes of hippocampal neurons were evaluated by hematoxylin-eosin (HE) staining; the contents of IL-1, IL-6, IL-10 and TNF-alpha, and the NF- kappa B expression were measured by enzyme-linked immunosorbent assay (ELISA) and immunohistochemical staining. The superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were also detected.
The SLM function and hippocampal neurons were significantly impaired after the occurrence of GCIRI. The MDA, IL-1, IL-6, IL-10, TNF-alpha content and expression of PPARs increased significantly, but the SOD activity and NF-kappa B expression were weakened in the hippocampus. Rosiglitazone treatment significantly protected rats from SLM function impairment and neuron death, and resulted in higher expressions of SOD activity and NF-kappa B, but lower contents of MDA and inflammatory factors. After treatment with rosiglitazone or GW9662, no significant change in PPAR-alpha or -beta expression was detected.
Rosiglitazone, a PPAR-gamma agonist, plays a protective role in hippocampal neuron damage of GCIRI rats by inhibiting the oxidative stress response and inflammation. The activation or antagonism of PPAR-gamma did not affect the expression of PPAR-alpha or -beta, indicating that the three subtypes of PPARs act in independent pathways in the CNS. |
doi_str_mv | 10.1186/1744-9081-10-21 |
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A rat GCIRI model was established by occlusion of bilateral common carotid arteries and cervical vena retransfusion. GW9662 (5 μg), a selective PPAR- gamma antagonist, was intraventricularly injected at 0.5 h before GCIR; Rosiglitazone (0.8, 2.4 and 7.2 mg/kg), a selective PPAR- gamma agonist, was injected intraperitoneally at 1 h before GCIRI. The expression changes of PPAR-alpha, -beta and -gamma at mRNA and protein levels were detected by RT-PCR and western blotting. The changes of spatial learning and memory (SLM) functions were assessed by using a Morris water maze; the pathohistological changes of hippocampal neurons were evaluated by hematoxylin-eosin (HE) staining; the contents of IL-1, IL-6, IL-10 and TNF-alpha, and the NF- kappa B expression were measured by enzyme-linked immunosorbent assay (ELISA) and immunohistochemical staining. The superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were also detected.
The SLM function and hippocampal neurons were significantly impaired after the occurrence of GCIRI. The MDA, IL-1, IL-6, IL-10, TNF-alpha content and expression of PPARs increased significantly, but the SOD activity and NF-kappa B expression were weakened in the hippocampus. Rosiglitazone treatment significantly protected rats from SLM function impairment and neuron death, and resulted in higher expressions of SOD activity and NF-kappa B, but lower contents of MDA and inflammatory factors. After treatment with rosiglitazone or GW9662, no significant change in PPAR-alpha or -beta expression was detected.
Rosiglitazone, a PPAR-gamma agonist, plays a protective role in hippocampal neuron damage of GCIRI rats by inhibiting the oxidative stress response and inflammation. The activation or antagonism of PPAR-gamma did not affect the expression of PPAR-alpha or -beta, indicating that the three subtypes of PPARs act in independent pathways in the CNS.</description><identifier>ISSN: 1744-9081</identifier><identifier>EISSN: 1744-9081</identifier><identifier>DOI: 10.1186/1744-9081-10-21</identifier><identifier>PMID: 24934302</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Analysis ; Animals ; Brain damage ; Cell adhesion & migration ; Cell cycle ; Cytokines - metabolism ; Deoxyribonucleic acid ; DNA ; Gene expression ; Hippocampus - metabolism ; Hippocampus - physiopathology ; Ischemia ; Laboratory animals ; Ligands ; Male ; Medical research ; Medicine, Experimental ; Memory ; Memory - physiology ; Metabolism ; Neurons ; Neurons - metabolism ; NF-kappa B - metabolism ; Oxidative stress ; Physiological aspects ; PPAR alpha - genetics ; PPAR alpha - metabolism ; PPAR gamma - genetics ; PPAR gamma - metabolism ; PPAR-beta - genetics ; PPAR-beta - metabolism ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury - metabolism ; Reperfusion Injury - physiopathology ; Rodents ; Spatial Learning - physiology ; Superoxide Dismutase - metabolism ; Veins & arteries</subject><ispartof>Behavioral and Brain Functions, 2014-06, Vol.10 (1), p.21-21, Article 21</ispartof><rights>COPYRIGHT 2014 BioMed Central Ltd.</rights><rights>2014 Luo et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.</rights><rights>Copyright © 2014 Luo et al.; licensee BioMed Central Ltd. 2014 Luo et al.; licensee BioMed Central Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b680t-1f0637374ad269d2c61dcaf275944ff0b0b2881fe8a55c3ac402c280732b68f03</citedby><cites>FETCH-LOGICAL-b680t-1f0637374ad269d2c61dcaf275944ff0b0b2881fe8a55c3ac402c280732b68f03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4167308/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4167308/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24934302$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Luo, Ying</creatorcontrib><creatorcontrib>He, Qin</creatorcontrib><creatorcontrib>Kuang, Ge</creatorcontrib><creatorcontrib>Jiang, Qingsong</creatorcontrib><creatorcontrib>Yang, Junqing</creatorcontrib><title>PPAR-alpha and PPAR-beta expression changes in the hippocampus of rats undergoing global cerebral ischemia/reperfusion due to PPAR-gamma status</title><title>Behavioral and Brain Functions</title><addtitle>Behav Brain Funct</addtitle><description>Peroxisome proliferator-activated receptors (PPARs, including alpha, beta and gamma subtypes) and their agonists have a protective role in treatment of central nervous system (CNS) diseases. The present study was designed to investigate the expression changes of PPAR-alpha, -beta, -gamma and NF-kappa B in the hippocampus of rats with global cerebral ischemia/reperfusion injury (GCIRI) after treatment with agonists or antagonists of PPAR-gamma.
A rat GCIRI model was established by occlusion of bilateral common carotid arteries and cervical vena retransfusion. GW9662 (5 μg), a selective PPAR- gamma antagonist, was intraventricularly injected at 0.5 h before GCIR; Rosiglitazone (0.8, 2.4 and 7.2 mg/kg), a selective PPAR- gamma agonist, was injected intraperitoneally at 1 h before GCIRI. The expression changes of PPAR-alpha, -beta and -gamma at mRNA and protein levels were detected by RT-PCR and western blotting. The changes of spatial learning and memory (SLM) functions were assessed by using a Morris water maze; the pathohistological changes of hippocampal neurons were evaluated by hematoxylin-eosin (HE) staining; the contents of IL-1, IL-6, IL-10 and TNF-alpha, and the NF- kappa B expression were measured by enzyme-linked immunosorbent assay (ELISA) and immunohistochemical staining. The superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were also detected.
The SLM function and hippocampal neurons were significantly impaired after the occurrence of GCIRI. The MDA, IL-1, IL-6, IL-10, TNF-alpha content and expression of PPARs increased significantly, but the SOD activity and NF-kappa B expression were weakened in the hippocampus. Rosiglitazone treatment significantly protected rats from SLM function impairment and neuron death, and resulted in higher expressions of SOD activity and NF-kappa B, but lower contents of MDA and inflammatory factors. After treatment with rosiglitazone or GW9662, no significant change in PPAR-alpha or -beta expression was detected.
Rosiglitazone, a PPAR-gamma agonist, plays a protective role in hippocampal neuron damage of GCIRI rats by inhibiting the oxidative stress response and inflammation. The activation or antagonism of PPAR-gamma did not affect the expression of PPAR-alpha or -beta, indicating that the three subtypes of PPARs act in independent pathways in the CNS.</description><subject>Analysis</subject><subject>Animals</subject><subject>Brain damage</subject><subject>Cell adhesion & migration</subject><subject>Cell cycle</subject><subject>Cytokines - metabolism</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>Gene expression</subject><subject>Hippocampus - metabolism</subject><subject>Hippocampus - physiopathology</subject><subject>Ischemia</subject><subject>Laboratory animals</subject><subject>Ligands</subject><subject>Male</subject><subject>Medical research</subject><subject>Medicine, Experimental</subject><subject>Memory</subject><subject>Memory - physiology</subject><subject>Metabolism</subject><subject>Neurons</subject><subject>Neurons - metabolism</subject><subject>NF-kappa B - metabolism</subject><subject>Oxidative stress</subject><subject>Physiological aspects</subject><subject>PPAR alpha - genetics</subject><subject>PPAR alpha - metabolism</subject><subject>PPAR gamma - genetics</subject><subject>PPAR gamma - metabolism</subject><subject>PPAR-beta - genetics</subject><subject>PPAR-beta - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reperfusion Injury - metabolism</subject><subject>Reperfusion Injury - physiopathology</subject><subject>Rodents</subject><subject>Spatial Learning - physiology</subject><subject>Superoxide Dismutase - metabolism</subject><subject>Veins & arteries</subject><issn>1744-9081</issn><issn>1744-9081</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</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>eNqNUktv1DAQjhCIlsKZG7LEhUu6fsVxLkjbipdUiQrB2XKcceIqsYOdIPgV_GW8u2XVIpCQDx7PfPP5m0dRPCf4nBApNqTmvGywJCXBJSUPitOj5-Ed-6R4ktINxkxySh8XJ5Q3jDNMT4uf19fbT6Ue50Ej7Tu0f7awaATf5wgpueCRGbTvISHn0TIAGtw8B6OneU0oWBT1ktDqO4h9cL5H_RhaPSIDEdqYDZfMAJPTmwgzRLvuKbsV0BIO3_V6mjRKi17W9LR4ZPWY4NntfVZ8efvm8-X78urjuw-X26uyFRIvJbFYsJrVXHdUNB01gnRGW1pXDefW4ha3VEpiQeqqMkwbjqmhEteMZgKL2Vnx-sA7r-0EnQG_ZK1qjm7S8YcK2qn7Ee8G1YdvihNRMywzwcWBoHXhHwT3IyZMajcQtRuIIlhRkkle3aqI4esKaVFT7haMo_YQ1qRIJYRktRT_BWVNwyq2k_byD-hNWKPP7dyjmBSy3qHOD6hej6CctyHLNPl0eVgmeLAu-7cVx4JjznlO2BwSTAwpRbDHYnMxu238S3kv7jb5iP-9fuwX9yPbYA</recordid><startdate>20140616</startdate><enddate>20140616</enddate><creator>Luo, Ying</creator><creator>He, Qin</creator><creator>Kuang, Ge</creator><creator>Jiang, Qingsong</creator><creator>Yang, Junqing</creator><general>BioMed Central Ltd</general><general>BioMed Central</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>IAO</scope><scope>3V.</scope><scope>7QG</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</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>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20140616</creationdate><title>PPAR-alpha and PPAR-beta expression changes in the hippocampus of rats undergoing global cerebral ischemia/reperfusion due to PPAR-gamma status</title><author>Luo, Ying ; He, Qin ; Kuang, Ge ; Jiang, Qingsong ; Yang, Junqing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b680t-1f0637374ad269d2c61dcaf275944ff0b0b2881fe8a55c3ac402c280732b68f03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Analysis</topic><topic>Animals</topic><topic>Brain damage</topic><topic>Cell adhesion & migration</topic><topic>Cell cycle</topic><topic>Cytokines - metabolism</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>Gene expression</topic><topic>Hippocampus - metabolism</topic><topic>Hippocampus - physiopathology</topic><topic>Ischemia</topic><topic>Laboratory animals</topic><topic>Ligands</topic><topic>Male</topic><topic>Medical research</topic><topic>Medicine, Experimental</topic><topic>Memory</topic><topic>Memory - physiology</topic><topic>Metabolism</topic><topic>Neurons</topic><topic>Neurons - metabolism</topic><topic>NF-kappa B - metabolism</topic><topic>Oxidative stress</topic><topic>Physiological aspects</topic><topic>PPAR alpha - genetics</topic><topic>PPAR alpha - metabolism</topic><topic>PPAR gamma - genetics</topic><topic>PPAR gamma - metabolism</topic><topic>PPAR-beta - genetics</topic><topic>PPAR-beta - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reperfusion Injury - metabolism</topic><topic>Reperfusion Injury - physiopathology</topic><topic>Rodents</topic><topic>Spatial Learning - physiology</topic><topic>Superoxide Dismutase - metabolism</topic><topic>Veins & arteries</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Luo, Ying</creatorcontrib><creatorcontrib>He, Qin</creatorcontrib><creatorcontrib>Kuang, Ge</creatorcontrib><creatorcontrib>Jiang, Qingsong</creatorcontrib><creatorcontrib>Yang, Junqing</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale Academic OneFile</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</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>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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Psychology Database</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 One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Behavioral and Brain Functions</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Luo, Ying</au><au>He, Qin</au><au>Kuang, Ge</au><au>Jiang, Qingsong</au><au>Yang, Junqing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>PPAR-alpha and PPAR-beta expression changes in the hippocampus of rats undergoing global cerebral ischemia/reperfusion due to PPAR-gamma status</atitle><jtitle>Behavioral and Brain Functions</jtitle><addtitle>Behav Brain Funct</addtitle><date>2014-06-16</date><risdate>2014</risdate><volume>10</volume><issue>1</issue><spage>21</spage><epage>21</epage><pages>21-21</pages><artnum>21</artnum><issn>1744-9081</issn><eissn>1744-9081</eissn><abstract>Peroxisome proliferator-activated receptors (PPARs, including alpha, beta and gamma subtypes) and their agonists have a protective role in treatment of central nervous system (CNS) diseases. The present study was designed to investigate the expression changes of PPAR-alpha, -beta, -gamma and NF-kappa B in the hippocampus of rats with global cerebral ischemia/reperfusion injury (GCIRI) after treatment with agonists or antagonists of PPAR-gamma.
A rat GCIRI model was established by occlusion of bilateral common carotid arteries and cervical vena retransfusion. GW9662 (5 μg), a selective PPAR- gamma antagonist, was intraventricularly injected at 0.5 h before GCIR; Rosiglitazone (0.8, 2.4 and 7.2 mg/kg), a selective PPAR- gamma agonist, was injected intraperitoneally at 1 h before GCIRI. The expression changes of PPAR-alpha, -beta and -gamma at mRNA and protein levels were detected by RT-PCR and western blotting. The changes of spatial learning and memory (SLM) functions were assessed by using a Morris water maze; the pathohistological changes of hippocampal neurons were evaluated by hematoxylin-eosin (HE) staining; the contents of IL-1, IL-6, IL-10 and TNF-alpha, and the NF- kappa B expression were measured by enzyme-linked immunosorbent assay (ELISA) and immunohistochemical staining. The superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were also detected.
The SLM function and hippocampal neurons were significantly impaired after the occurrence of GCIRI. The MDA, IL-1, IL-6, IL-10, TNF-alpha content and expression of PPARs increased significantly, but the SOD activity and NF-kappa B expression were weakened in the hippocampus. Rosiglitazone treatment significantly protected rats from SLM function impairment and neuron death, and resulted in higher expressions of SOD activity and NF-kappa B, but lower contents of MDA and inflammatory factors. After treatment with rosiglitazone or GW9662, no significant change in PPAR-alpha or -beta expression was detected.
Rosiglitazone, a PPAR-gamma agonist, plays a protective role in hippocampal neuron damage of GCIRI rats by inhibiting the oxidative stress response and inflammation. The activation or antagonism of PPAR-gamma did not affect the expression of PPAR-alpha or -beta, indicating that the three subtypes of PPARs act in independent pathways in the CNS.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>24934302</pmid><doi>10.1186/1744-9081-10-21</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Analysis Animals Brain damage Cell adhesion & migration Cell cycle Cytokines - metabolism Deoxyribonucleic acid DNA Gene expression Hippocampus - metabolism Hippocampus - physiopathology Ischemia Laboratory animals Ligands Male Medical research Medicine, Experimental Memory Memory - physiology Metabolism Neurons Neurons - metabolism NF-kappa B - metabolism Oxidative stress Physiological aspects PPAR alpha - genetics PPAR alpha - metabolism PPAR gamma - genetics PPAR gamma - metabolism PPAR-beta - genetics PPAR-beta - metabolism Rats Rats, Sprague-Dawley Reperfusion Injury - metabolism Reperfusion Injury - physiopathology Rodents Spatial Learning - physiology Superoxide Dismutase - metabolism Veins & arteries |
title | PPAR-alpha and PPAR-beta expression changes in the hippocampus of rats undergoing global cerebral ischemia/reperfusion due to PPAR-gamma status |
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