Does Glp-2 have a protective effect on cerebral ischemia/reperfusion model?
To investigate the neuroprotective effects of glucagon-like peptide 2 (Glp-2), which increases cerebral blood flow, on the hippocampal complex after cerebral ischemia/reperfusion (I/R) injury in rats. Animals were randomized into 4 groups: sham, I/R + 0.9% NaCl, I/R + pre-Glp-2, and I/R + post-Glp-2...
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| Veröffentlicht in: | Turkish journal of medical sciences 2015, Vol.45 (3), p.467-473 |
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| container_title | Turkish journal of medical sciences |
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| creator | Topaloğlu, Naci Memi, Gülsün Kaner, Tuncay Deniz, Mustafa Şahin, Önder Güven, Mustafa Çoşar, Murat |
| description | To investigate the neuroprotective effects of glucagon-like peptide 2 (Glp-2), which increases cerebral blood flow, on the hippocampal complex after cerebral ischemia/reperfusion (I/R) injury in rats.
Animals were randomized into 4 groups: sham, I/R + 0.9% NaCl, I/R + pre-Glp-2, and I/R + post-Glp-2. Cerebral ischemia was performed via the occlusion of the bilateral internal carotid artery for 40 min and continued with a reperfusion process. At the end of 6 h of reperfusion, animals were decapitated in all groups and brain tissues were removed. Malondialdehyde (MDA) and natural intracellular antioxidant glutathione (GSH) levels and myeloperoxidase (MPO) activities were measured in the left hippocampal tissue. The right hippocampal tissues of all group members were taken for histopathologic study.
MDA levels and MPO activities increased from Group I to Group II and decreased from Group II to Groups III and IV. On the other hand, GSH levels were not significantly different among the groups. The number of apoptotic hippocampal tissue cells increased from Group I to Group II and decreased from Group II to Groups III and IV.
Our preliminary study revealed that Glp-2 treatment may decrease oxidative damage from I/R in cerebral tissue. |
| doi_str_mv | 10.3906/sag-1402-64 |
| format | Article |
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Animals were randomized into 4 groups: sham, I/R + 0.9% NaCl, I/R + pre-Glp-2, and I/R + post-Glp-2. Cerebral ischemia was performed via the occlusion of the bilateral internal carotid artery for 40 min and continued with a reperfusion process. At the end of 6 h of reperfusion, animals were decapitated in all groups and brain tissues were removed. Malondialdehyde (MDA) and natural intracellular antioxidant glutathione (GSH) levels and myeloperoxidase (MPO) activities were measured in the left hippocampal tissue. The right hippocampal tissues of all group members were taken for histopathologic study.
MDA levels and MPO activities increased from Group I to Group II and decreased from Group II to Groups III and IV. On the other hand, GSH levels were not significantly different among the groups. The number of apoptotic hippocampal tissue cells increased from Group I to Group II and decreased from Group II to Groups III and IV.
Our preliminary study revealed that Glp-2 treatment may decrease oxidative damage from I/R in cerebral tissue.</description><identifier>ISSN: 1300-0144</identifier><identifier>EISSN: 1303-6165</identifier><identifier>DOI: 10.3906/sag-1402-64</identifier><identifier>PMID: 26281308</identifier><language>eng</language><publisher>Turkey</publisher><subject>Animals ; Apoptosis - drug effects ; Brain Ischemia - metabolism ; Brain Ischemia - pathology ; Cell Death - drug effects ; Disease Models, Animal ; Glucagon-Like Peptide 2 - pharmacology ; Glutathione - drug effects ; Glutathione - metabolism ; Hippocampus - drug effects ; Hippocampus - metabolism ; Male ; Malondialdehyde - metabolism ; Neuroprotective Agents - pharmacology ; Oxidative Stress - drug effects ; Peroxidase - drug effects ; Peroxidase - metabolism ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury - metabolism ; Reperfusion Injury - prevention & control ; Superoxide Dismutase - drug effects ; Superoxide Dismutase - metabolism</subject><ispartof>Turkish journal of medical sciences, 2015, Vol.45 (3), p.467-473</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c326t-7040a575fea7bfdb989b2009d93800a68bb8ea741b90c626cad181c89ca869aa3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,4024,27923,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26281308$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Topaloğlu, Naci</creatorcontrib><creatorcontrib>Memi, Gülsün</creatorcontrib><creatorcontrib>Kaner, Tuncay</creatorcontrib><creatorcontrib>Deniz, Mustafa</creatorcontrib><creatorcontrib>Şahin, Önder</creatorcontrib><creatorcontrib>Güven, Mustafa</creatorcontrib><creatorcontrib>Çoşar, Murat</creatorcontrib><title>Does Glp-2 have a protective effect on cerebral ischemia/reperfusion model?</title><title>Turkish journal of medical sciences</title><addtitle>Turk J Med Sci</addtitle><description>To investigate the neuroprotective effects of glucagon-like peptide 2 (Glp-2), which increases cerebral blood flow, on the hippocampal complex after cerebral ischemia/reperfusion (I/R) injury in rats.
Animals were randomized into 4 groups: sham, I/R + 0.9% NaCl, I/R + pre-Glp-2, and I/R + post-Glp-2. Cerebral ischemia was performed via the occlusion of the bilateral internal carotid artery for 40 min and continued with a reperfusion process. At the end of 6 h of reperfusion, animals were decapitated in all groups and brain tissues were removed. Malondialdehyde (MDA) and natural intracellular antioxidant glutathione (GSH) levels and myeloperoxidase (MPO) activities were measured in the left hippocampal tissue. The right hippocampal tissues of all group members were taken for histopathologic study.
MDA levels and MPO activities increased from Group I to Group II and decreased from Group II to Groups III and IV. On the other hand, GSH levels were not significantly different among the groups. The number of apoptotic hippocampal tissue cells increased from Group I to Group II and decreased from Group II to Groups III and IV.
Our preliminary study revealed that Glp-2 treatment may decrease oxidative damage from I/R in cerebral tissue.</description><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>Brain Ischemia - metabolism</subject><subject>Brain Ischemia - pathology</subject><subject>Cell Death - drug effects</subject><subject>Disease Models, Animal</subject><subject>Glucagon-Like Peptide 2 - pharmacology</subject><subject>Glutathione - drug effects</subject><subject>Glutathione - metabolism</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - metabolism</subject><subject>Male</subject><subject>Malondialdehyde - metabolism</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Oxidative Stress - drug effects</subject><subject>Peroxidase - drug effects</subject><subject>Peroxidase - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reperfusion Injury - metabolism</subject><subject>Reperfusion Injury - prevention & control</subject><subject>Superoxide Dismutase - drug effects</subject><subject>Superoxide Dismutase - metabolism</subject><issn>1300-0144</issn><issn>1303-6165</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kMFLwzAYxYMobk5P3qVHQeq-NGmanESmTnHgRc8hSb-6SrvWpBX8783c9PS9j_fj8XiEnFO4ZgrEPJj3lHLIUsEPyJQyYKmgIj_81ZAC5XxCTkL4AMgYz9UxmWQik9GUU_J812FIlk2fZsnafGFikt53A7qhjg9WVVRJt0kcerTeNEkd3Brb2sw99uirMdTRbbsSm5tTclSZJuDZ_s7I28P96-IxXb0snxa3q9SxTAxpARxMXuQVmsJWpVVS2QxAlYpJACOktTJanFoFTmTCmZJK6qRyRgplDJuRy11ubPo5Yhh0G1th05gNdmPQtICcF0JJiOjVDnW-C8FjpXtft8Z_awp6u56O6-ntelrwSF_sg0fbYvnP_s3FfgA402n5</recordid><startdate>2015</startdate><enddate>2015</enddate><creator>Topaloğlu, Naci</creator><creator>Memi, Gülsün</creator><creator>Kaner, Tuncay</creator><creator>Deniz, Mustafa</creator><creator>Şahin, Önder</creator><creator>Güven, Mustafa</creator><creator>Çoşar, Murat</creator><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>7X8</scope></search><sort><creationdate>2015</creationdate><title>Does Glp-2 have a protective effect on cerebral ischemia/reperfusion model?</title><author>Topaloğlu, Naci ; Memi, Gülsün ; Kaner, Tuncay ; Deniz, Mustafa ; Şahin, Önder ; Güven, Mustafa ; Çoşar, Murat</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c326t-7040a575fea7bfdb989b2009d93800a68bb8ea741b90c626cad181c89ca869aa3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Apoptosis - drug effects</topic><topic>Brain Ischemia - metabolism</topic><topic>Brain Ischemia - pathology</topic><topic>Cell Death - drug effects</topic><topic>Disease Models, Animal</topic><topic>Glucagon-Like Peptide 2 - pharmacology</topic><topic>Glutathione - drug effects</topic><topic>Glutathione - metabolism</topic><topic>Hippocampus - drug effects</topic><topic>Hippocampus - metabolism</topic><topic>Male</topic><topic>Malondialdehyde - metabolism</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Oxidative Stress - drug effects</topic><topic>Peroxidase - drug effects</topic><topic>Peroxidase - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reperfusion Injury - metabolism</topic><topic>Reperfusion Injury - prevention & control</topic><topic>Superoxide Dismutase - drug effects</topic><topic>Superoxide Dismutase - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Topaloğlu, Naci</creatorcontrib><creatorcontrib>Memi, Gülsün</creatorcontrib><creatorcontrib>Kaner, Tuncay</creatorcontrib><creatorcontrib>Deniz, Mustafa</creatorcontrib><creatorcontrib>Şahin, Önder</creatorcontrib><creatorcontrib>Güven, Mustafa</creatorcontrib><creatorcontrib>Çoşar, Murat</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Turkish journal of medical sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Topaloğlu, Naci</au><au>Memi, Gülsün</au><au>Kaner, Tuncay</au><au>Deniz, Mustafa</au><au>Şahin, Önder</au><au>Güven, Mustafa</au><au>Çoşar, Murat</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Does Glp-2 have a protective effect on cerebral ischemia/reperfusion model?</atitle><jtitle>Turkish journal of medical sciences</jtitle><addtitle>Turk J Med Sci</addtitle><date>2015</date><risdate>2015</risdate><volume>45</volume><issue>3</issue><spage>467</spage><epage>473</epage><pages>467-473</pages><issn>1300-0144</issn><eissn>1303-6165</eissn><abstract>To investigate the neuroprotective effects of glucagon-like peptide 2 (Glp-2), which increases cerebral blood flow, on the hippocampal complex after cerebral ischemia/reperfusion (I/R) injury in rats.
Animals were randomized into 4 groups: sham, I/R + 0.9% NaCl, I/R + pre-Glp-2, and I/R + post-Glp-2. Cerebral ischemia was performed via the occlusion of the bilateral internal carotid artery for 40 min and continued with a reperfusion process. At the end of 6 h of reperfusion, animals were decapitated in all groups and brain tissues were removed. Malondialdehyde (MDA) and natural intracellular antioxidant glutathione (GSH) levels and myeloperoxidase (MPO) activities were measured in the left hippocampal tissue. The right hippocampal tissues of all group members were taken for histopathologic study.
MDA levels and MPO activities increased from Group I to Group II and decreased from Group II to Groups III and IV. On the other hand, GSH levels were not significantly different among the groups. The number of apoptotic hippocampal tissue cells increased from Group I to Group II and decreased from Group II to Groups III and IV.
Our preliminary study revealed that Glp-2 treatment may decrease oxidative damage from I/R in cerebral tissue.</abstract><cop>Turkey</cop><pmid>26281308</pmid><doi>10.3906/sag-1402-64</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; TÜBİTAK Scientific Journals |
| subjects | Animals Apoptosis - drug effects Brain Ischemia - metabolism Brain Ischemia - pathology Cell Death - drug effects Disease Models, Animal Glucagon-Like Peptide 2 - pharmacology Glutathione - drug effects Glutathione - metabolism Hippocampus - drug effects Hippocampus - metabolism Male Malondialdehyde - metabolism Neuroprotective Agents - pharmacology Oxidative Stress - drug effects Peroxidase - drug effects Peroxidase - metabolism Rats Rats, Sprague-Dawley Reperfusion Injury - metabolism Reperfusion Injury - prevention & control Superoxide Dismutase - drug effects Superoxide Dismutase - metabolism |
| title | Does Glp-2 have a protective effect on cerebral ischemia/reperfusion model? |
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