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Effects of rosiglitazone on global ischemia-induced hippocampal injury and expression of mitochondrial uncoupling protein 2
We investigate the effect of rosiglitazone, a ligand for peroxisome proliferator-activated receptor-γ (PPARγ) with anti-inflammatory and anti-oxidative actions, on hippocampal injury and its roles in mitochondrial uncoupling protein 2 (UCP2) expression caused by transient global ischemia (TGI) in ra...
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| Published in: | Biochemical and biophysical research communications 2006-12, Vol.351 (1), p.198-203 |
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| Main Authors: | , , , , , , , |
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| cited_by | cdi_FETCH-LOGICAL-c413t-cd683270910ac84a84bca1b751a0136cc3d21f0b15cf8186f0efe1a412f270de3 |
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| cites | cdi_FETCH-LOGICAL-c413t-cd683270910ac84a84bca1b751a0136cc3d21f0b15cf8186f0efe1a412f270de3 |
| container_end_page | 203 |
| container_issue | 1 |
| container_start_page | 198 |
| container_title | Biochemical and biophysical research communications |
| container_volume | 351 |
| creator | Chen, Shang-Der Wu, Hsin-Yi Yang, Ding-I Lee, Su-Ying Shaw, Fu-Zen Lin, Tsu-Kung Liou, Chia-Wei Chuang, Yao-Chung |
| description | We investigate the effect of rosiglitazone, a ligand for peroxisome proliferator-activated receptor-γ (PPARγ) with anti-inflammatory and anti-oxidative actions, on hippocampal injury and its roles in mitochondrial uncoupling protein 2 (UCP2) expression caused by transient global ischemia (TGI) in rats. Increased UCP2 expression was observed in mitochondria of hippocampal CA1 2–24
h after TGI/reperfusion, with maximal expression levels at 6–18
h. Administration of rosiglitazone to hippocampus 30
min prior to the onset of TGI further enhanced mitochondrial UCP2 expression 2–6
h following TGI/reperfusion. Rats subjected to TGI/reperfusion displayed a significant increase in lipid peroxidation, based on increased malondialdehyde (MDA) levels, in hippocampal CA1 mitochondria 2–6 h after reperfusion. Rosiglitazone significantly attenuated TGI/reperfusion-induced lipid peroxidation and suppressed hippocampal CA1 neuronal death based on the surviving neuronal counts. In conclusion, our results provide correlative evidence for the “PPARγ
→
UCP2
→
neuroprotection” cascade in ischemic brain injury. |
| doi_str_mv | 10.1016/j.bbrc.2006.10.017 |
| format | article |
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h after TGI/reperfusion, with maximal expression levels at 6–18
h. Administration of rosiglitazone to hippocampus 30
min prior to the onset of TGI further enhanced mitochondrial UCP2 expression 2–6
h following TGI/reperfusion. Rats subjected to TGI/reperfusion displayed a significant increase in lipid peroxidation, based on increased malondialdehyde (MDA) levels, in hippocampal CA1 mitochondria 2–6 h after reperfusion. Rosiglitazone significantly attenuated TGI/reperfusion-induced lipid peroxidation and suppressed hippocampal CA1 neuronal death based on the surviving neuronal counts. In conclusion, our results provide correlative evidence for the “PPARγ
→
UCP2
→
neuroprotection” cascade in ischemic brain injury.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2006.10.017</identifier><identifier>PMID: 17052689</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>60 APPLIED LIFE SCIENCES ; Animals ; Global ischemia ; HIPPOCAMPUS ; Hippocampus - blood supply ; Hippocampus - drug effects ; Hippocampus - metabolism ; Hippocampus - pathology ; INFLAMMATION ; INJURIES ; Ion Channels - metabolism ; ISCHEMIA ; Ischemic Attack, Transient - metabolism ; Ischemic Attack, Transient - pathology ; LIGANDS ; LIPIDS ; Male ; MITOCHONDRIA ; Mitochondrial Proteins - metabolism ; Peroxisome proliferator-activated receptor-γ ; PPAR gamma - antagonists & inhibitors ; RATS ; Rats, Sprague-Dawley ; RECEPTORS ; Rosiglitazone ; Thiazolidinediones - pharmacology ; Uncoupling Protein 2</subject><ispartof>Biochemical and biophysical research communications, 2006-12, Vol.351 (1), p.198-203</ispartof><rights>2006 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c413t-cd683270910ac84a84bca1b751a0136cc3d21f0b15cf8186f0efe1a412f270de3</citedby><cites>FETCH-LOGICAL-c413t-cd683270910ac84a84bca1b751a0136cc3d21f0b15cf8186f0efe1a412f270de3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17052689$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://www.osti.gov/biblio/20857905$$D View this record in Osti.gov$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Shang-Der</creatorcontrib><creatorcontrib>Wu, Hsin-Yi</creatorcontrib><creatorcontrib>Yang, Ding-I</creatorcontrib><creatorcontrib>Lee, Su-Ying</creatorcontrib><creatorcontrib>Shaw, Fu-Zen</creatorcontrib><creatorcontrib>Lin, Tsu-Kung</creatorcontrib><creatorcontrib>Liou, Chia-Wei</creatorcontrib><creatorcontrib>Chuang, Yao-Chung</creatorcontrib><title>Effects of rosiglitazone on global ischemia-induced hippocampal injury and expression of mitochondrial uncoupling protein 2</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>We investigate the effect of rosiglitazone, a ligand for peroxisome proliferator-activated receptor-γ (PPARγ) with anti-inflammatory and anti-oxidative actions, on hippocampal injury and its roles in mitochondrial uncoupling protein 2 (UCP2) expression caused by transient global ischemia (TGI) in rats. Increased UCP2 expression was observed in mitochondria of hippocampal CA1 2–24
h after TGI/reperfusion, with maximal expression levels at 6–18
h. Administration of rosiglitazone to hippocampus 30
min prior to the onset of TGI further enhanced mitochondrial UCP2 expression 2–6
h following TGI/reperfusion. Rats subjected to TGI/reperfusion displayed a significant increase in lipid peroxidation, based on increased malondialdehyde (MDA) levels, in hippocampal CA1 mitochondria 2–6 h after reperfusion. Rosiglitazone significantly attenuated TGI/reperfusion-induced lipid peroxidation and suppressed hippocampal CA1 neuronal death based on the surviving neuronal counts. In conclusion, our results provide correlative evidence for the “PPARγ
→
UCP2
→
neuroprotection” cascade in ischemic brain injury.</description><subject>60 APPLIED LIFE SCIENCES</subject><subject>Animals</subject><subject>Global ischemia</subject><subject>HIPPOCAMPUS</subject><subject>Hippocampus - blood supply</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - metabolism</subject><subject>Hippocampus - pathology</subject><subject>INFLAMMATION</subject><subject>INJURIES</subject><subject>Ion Channels - metabolism</subject><subject>ISCHEMIA</subject><subject>Ischemic Attack, Transient - metabolism</subject><subject>Ischemic Attack, Transient - pathology</subject><subject>LIGANDS</subject><subject>LIPIDS</subject><subject>Male</subject><subject>MITOCHONDRIA</subject><subject>Mitochondrial Proteins - metabolism</subject><subject>Peroxisome proliferator-activated receptor-γ</subject><subject>PPAR gamma - antagonists & inhibitors</subject><subject>RATS</subject><subject>Rats, Sprague-Dawley</subject><subject>RECEPTORS</subject><subject>Rosiglitazone</subject><subject>Thiazolidinediones - pharmacology</subject><subject>Uncoupling Protein 2</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><recordid>eNqFkc2LFDEQxYMo7rj6D3iQgOCtx6r0Z8CLLOsHLHhR8BbS6cpMhu6kTbplV_9508yANz0Fqn7vkVePsZcIewRs3p72fR_NXgA0ebAHbB-xHYKEQiBUj9kO8qYQEr9fsWcpnQAQq0Y-ZVfYQi2aTu7Y71trySyJB8tjSO4wukX_Cp548Pwwhl6P3CVzpMnpwvlhNTTwo5vnYPQ0b0t_WuMD137gdD9HSsllZXab3BLMMfghuoyt3oR1Hp0_8DmGhZzn4jl7YvWY6MXlvWbfPtx-vflU3H35-Pnm_V1hKiyXwgxNV4oWJII2XaW7qjca-7ZGDVg2xpSDQAs91sZ22DUWyBLqCoXNqoHKa_b67BvS4lQybiFzNMH7HFwJ6OpWQp2pN2cq_-_HSmlRUw5O46g9hTWpRuabg-z-C6IsO1FVTQbFGTT5simSVXN0k44PCkFtDaqT2hpUW4PbLDeYRa8u7ms_0fBXcqksA-_OAOWT_XQUt0Tkcy8uboGG4P7l_weK6655</recordid><startdate>20061208</startdate><enddate>20061208</enddate><creator>Chen, Shang-Der</creator><creator>Wu, Hsin-Yi</creator><creator>Yang, Ding-I</creator><creator>Lee, Su-Ying</creator><creator>Shaw, Fu-Zen</creator><creator>Lin, Tsu-Kung</creator><creator>Liou, Chia-Wei</creator><creator>Chuang, Yao-Chung</creator><general>Elsevier Inc</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>7TK</scope><scope>7X8</scope><scope>OTOTI</scope></search><sort><creationdate>20061208</creationdate><title>Effects of rosiglitazone on global ischemia-induced hippocampal injury and expression of mitochondrial uncoupling protein 2</title><author>Chen, Shang-Der ; Wu, Hsin-Yi ; Yang, Ding-I ; Lee, Su-Ying ; Shaw, Fu-Zen ; Lin, Tsu-Kung ; Liou, Chia-Wei ; Chuang, Yao-Chung</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c413t-cd683270910ac84a84bca1b751a0136cc3d21f0b15cf8186f0efe1a412f270de3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>60 APPLIED LIFE SCIENCES</topic><topic>Animals</topic><topic>Global ischemia</topic><topic>HIPPOCAMPUS</topic><topic>Hippocampus - blood supply</topic><topic>Hippocampus - drug effects</topic><topic>Hippocampus - metabolism</topic><topic>Hippocampus - pathology</topic><topic>INFLAMMATION</topic><topic>INJURIES</topic><topic>Ion Channels - metabolism</topic><topic>ISCHEMIA</topic><topic>Ischemic Attack, Transient - metabolism</topic><topic>Ischemic Attack, Transient - pathology</topic><topic>LIGANDS</topic><topic>LIPIDS</topic><topic>Male</topic><topic>MITOCHONDRIA</topic><topic>Mitochondrial Proteins - metabolism</topic><topic>Peroxisome proliferator-activated receptor-γ</topic><topic>PPAR gamma - antagonists & inhibitors</topic><topic>RATS</topic><topic>Rats, Sprague-Dawley</topic><topic>RECEPTORS</topic><topic>Rosiglitazone</topic><topic>Thiazolidinediones - pharmacology</topic><topic>Uncoupling Protein 2</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Shang-Der</creatorcontrib><creatorcontrib>Wu, Hsin-Yi</creatorcontrib><creatorcontrib>Yang, Ding-I</creatorcontrib><creatorcontrib>Lee, Su-Ying</creatorcontrib><creatorcontrib>Shaw, Fu-Zen</creatorcontrib><creatorcontrib>Lin, Tsu-Kung</creatorcontrib><creatorcontrib>Liou, Chia-Wei</creatorcontrib><creatorcontrib>Chuang, Yao-Chung</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><collection>OSTI.GOV</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Shang-Der</au><au>Wu, Hsin-Yi</au><au>Yang, Ding-I</au><au>Lee, Su-Ying</au><au>Shaw, Fu-Zen</au><au>Lin, Tsu-Kung</au><au>Liou, Chia-Wei</au><au>Chuang, Yao-Chung</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of rosiglitazone on global ischemia-induced hippocampal injury and expression of mitochondrial uncoupling protein 2</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2006-12-08</date><risdate>2006</risdate><volume>351</volume><issue>1</issue><spage>198</spage><epage>203</epage><pages>198-203</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>We investigate the effect of rosiglitazone, a ligand for peroxisome proliferator-activated receptor-γ (PPARγ) with anti-inflammatory and anti-oxidative actions, on hippocampal injury and its roles in mitochondrial uncoupling protein 2 (UCP2) expression caused by transient global ischemia (TGI) in rats. Increased UCP2 expression was observed in mitochondria of hippocampal CA1 2–24
h after TGI/reperfusion, with maximal expression levels at 6–18
h. Administration of rosiglitazone to hippocampus 30
min prior to the onset of TGI further enhanced mitochondrial UCP2 expression 2–6
h following TGI/reperfusion. Rats subjected to TGI/reperfusion displayed a significant increase in lipid peroxidation, based on increased malondialdehyde (MDA) levels, in hippocampal CA1 mitochondria 2–6 h after reperfusion. Rosiglitazone significantly attenuated TGI/reperfusion-induced lipid peroxidation and suppressed hippocampal CA1 neuronal death based on the surviving neuronal counts. In conclusion, our results provide correlative evidence for the “PPARγ
→
UCP2
→
neuroprotection” cascade in ischemic brain injury.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>17052689</pmid><doi>10.1016/j.bbrc.2006.10.017</doi><tpages>6</tpages></addata></record> |
| fulltext | fulltext |
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| ispartof | Biochemical and biophysical research communications, 2006-12, Vol.351 (1), p.198-203 |
| issn | 0006-291X 1090-2104 |
| language | eng |
| recordid | cdi_osti_scitechconnect_20857905 |
| source | ScienceDirect Freedom Collection 2022-2024 |
| subjects | 60 APPLIED LIFE SCIENCES Animals Global ischemia HIPPOCAMPUS Hippocampus - blood supply Hippocampus - drug effects Hippocampus - metabolism Hippocampus - pathology INFLAMMATION INJURIES Ion Channels - metabolism ISCHEMIA Ischemic Attack, Transient - metabolism Ischemic Attack, Transient - pathology LIGANDS LIPIDS Male MITOCHONDRIA Mitochondrial Proteins - metabolism Peroxisome proliferator-activated receptor-γ PPAR gamma - antagonists & inhibitors RATS Rats, Sprague-Dawley RECEPTORS Rosiglitazone Thiazolidinediones - pharmacology Uncoupling Protein 2 |
| title | Effects of rosiglitazone on global ischemia-induced hippocampal injury and expression of mitochondrial uncoupling protein 2 |
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