Effects of Sulphasalazine in Cerebral Ischemia Reperfusion Injury in Rat
Management of cerebral ischemia/reperfusion (I/R) injury is still difficult process today. Aim of present study was to investigate therapeutic properties of sulfasalazine in cerebral transient I/R injury in rat. Except Control group (n = 5), 20 Wistar albino rats were allocated for acute and chronic...
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| Veröffentlicht in: | Archives of medical research 2017-04, Vol.48 (3), p.247-256 |
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| creator | Cetin, Cansel Erdogan, Ahmet Melih Dincel, Gungor Cagdas Bakar, Bulent Kisa, Ucler |
| description | Management of cerebral ischemia/reperfusion (I/R) injury is still difficult process today.
Aim of present study was to investigate therapeutic properties of sulfasalazine in cerebral transient I/R injury in rat.
Except Control group (n = 5), 20 Wistar albino rats were allocated for acute and chronic stage investigation of I/R injury, and temporary aneurysm clips were attempted to both internal carotid arteries for thirty min. Four hours later, 40 mg/kg once a day sulfasalazine was administered to animals of SL-A and SL-C groups, orally. Animals were decapitated, following which pyknotic and necrotic neuronal cells, perivascular edema, irregularities of intercellular organization (IIO) of hippocampal regions, and cortical necrotic neurons of parietal lobe were counted or scaled histopathologically. Tissue malonyldialdehyde (MDA), myeloperoxidation (MPO), total nitrite/nitrate (NO), interleukin 1-beta (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) level values were evaluated biochemically.
Sulfasalazine could reduce perivascular edema, IIO, cortical and hippocampal neuronal cell death in both stages. It could decrease MDA in acute stage, but not reduce IL-1β, IL-6, MPO, NO, and TNFα levels. It could increase IL-1β levels in chronic stage but not affect to IL-6, MPO, MDA, NO, TNF-α levels.
Sulfasalazine could improve histopathological architecture of hypoxic tissue in both stages of I/R injury in rat. It could inhibit lipid peroxidation cascades just in acute stage. These results suggested that therapeutic mechanisms of sulfasalazine in cerebral I/R injury should be investigated by using more specific laboratory methods in future studies. |
| doi_str_mv | 10.1016/j.arcmed.2017.06.004 |
| format | Article |
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Aim of present study was to investigate therapeutic properties of sulfasalazine in cerebral transient I/R injury in rat.
Except Control group (n = 5), 20 Wistar albino rats were allocated for acute and chronic stage investigation of I/R injury, and temporary aneurysm clips were attempted to both internal carotid arteries for thirty min. Four hours later, 40 mg/kg once a day sulfasalazine was administered to animals of SL-A and SL-C groups, orally. Animals were decapitated, following which pyknotic and necrotic neuronal cells, perivascular edema, irregularities of intercellular organization (IIO) of hippocampal regions, and cortical necrotic neurons of parietal lobe were counted or scaled histopathologically. Tissue malonyldialdehyde (MDA), myeloperoxidation (MPO), total nitrite/nitrate (NO), interleukin 1-beta (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) level values were evaluated biochemically.
Sulfasalazine could reduce perivascular edema, IIO, cortical and hippocampal neuronal cell death in both stages. It could decrease MDA in acute stage, but not reduce IL-1β, IL-6, MPO, NO, and TNFα levels. It could increase IL-1β levels in chronic stage but not affect to IL-6, MPO, MDA, NO, TNF-α levels.
Sulfasalazine could improve histopathological architecture of hypoxic tissue in both stages of I/R injury in rat. It could inhibit lipid peroxidation cascades just in acute stage. These results suggested that therapeutic mechanisms of sulfasalazine in cerebral I/R injury should be investigated by using more specific laboratory methods in future studies.</description><identifier>ISSN: 0188-4409</identifier><identifier>EISSN: 1873-5487</identifier><identifier>DOI: 10.1016/j.arcmed.2017.06.004</identifier><identifier>PMID: 28923326</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Anti-Inflammatory Agents, Non-Steroidal - therapeutic use ; Antiinflamatory ; Brain Edema - drug therapy ; Brain Edema - metabolism ; Brain Ischemia - drug therapy ; Brain Ischemia - metabolism ; Brain Ischemia - pathology ; Cerebral Cortex - drug effects ; Cerebral Cortex - metabolism ; Cerebral Cortex - pathology ; Cerebral hypoxia reperfusion injury ; Hippocampus - drug effects ; Hippocampus - metabolism ; Hippocampus - pathology ; Interleukin-1beta - metabolism ; Interleukin-6 - metabolism ; Lipid Peroxidation - drug effects ; Male ; Malondialdehyde - metabolism ; Nitric Oxide - metabolism ; Peroxidase - metabolism ; Rats, Wistar ; Reperfusion Injury - drug therapy ; Reperfusion Injury - metabolism ; Reperfusion Injury - pathology ; Stroke ; Sulfasalazine ; Sulfasalazine - therapeutic use ; Tumor Necrosis Factor-alpha - metabolism</subject><ispartof>Archives of medical research, 2017-04, Vol.48 (3), p.247-256</ispartof><rights>2017 IMSS</rights><rights>Copyright © 2017 IMSS. Published by Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c362t-6826eee4b3edcee7e8b5771b2adfebb550a86874e3149ac553add3f3bb69ea33</citedby><cites>FETCH-LOGICAL-c362t-6826eee4b3edcee7e8b5771b2adfebb550a86874e3149ac553add3f3bb69ea33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.arcmed.2017.06.004$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28923326$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cetin, Cansel</creatorcontrib><creatorcontrib>Erdogan, Ahmet Melih</creatorcontrib><creatorcontrib>Dincel, Gungor Cagdas</creatorcontrib><creatorcontrib>Bakar, Bulent</creatorcontrib><creatorcontrib>Kisa, Ucler</creatorcontrib><title>Effects of Sulphasalazine in Cerebral Ischemia Reperfusion Injury in Rat</title><title>Archives of medical research</title><addtitle>Arch Med Res</addtitle><description>Management of cerebral ischemia/reperfusion (I/R) injury is still difficult process today.
Aim of present study was to investigate therapeutic properties of sulfasalazine in cerebral transient I/R injury in rat.
Except Control group (n = 5), 20 Wistar albino rats were allocated for acute and chronic stage investigation of I/R injury, and temporary aneurysm clips were attempted to both internal carotid arteries for thirty min. Four hours later, 40 mg/kg once a day sulfasalazine was administered to animals of SL-A and SL-C groups, orally. Animals were decapitated, following which pyknotic and necrotic neuronal cells, perivascular edema, irregularities of intercellular organization (IIO) of hippocampal regions, and cortical necrotic neurons of parietal lobe were counted or scaled histopathologically. Tissue malonyldialdehyde (MDA), myeloperoxidation (MPO), total nitrite/nitrate (NO), interleukin 1-beta (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) level values were evaluated biochemically.
Sulfasalazine could reduce perivascular edema, IIO, cortical and hippocampal neuronal cell death in both stages. It could decrease MDA in acute stage, but not reduce IL-1β, IL-6, MPO, NO, and TNFα levels. It could increase IL-1β levels in chronic stage but not affect to IL-6, MPO, MDA, NO, TNF-α levels.
Sulfasalazine could improve histopathological architecture of hypoxic tissue in both stages of I/R injury in rat. It could inhibit lipid peroxidation cascades just in acute stage. These results suggested that therapeutic mechanisms of sulfasalazine in cerebral I/R injury should be investigated by using more specific laboratory methods in future studies.</description><subject>Animals</subject><subject>Anti-Inflammatory Agents, Non-Steroidal - therapeutic use</subject><subject>Antiinflamatory</subject><subject>Brain Edema - drug therapy</subject><subject>Brain Edema - metabolism</subject><subject>Brain Ischemia - drug therapy</subject><subject>Brain Ischemia - metabolism</subject><subject>Brain Ischemia - pathology</subject><subject>Cerebral Cortex - drug effects</subject><subject>Cerebral Cortex - metabolism</subject><subject>Cerebral Cortex - pathology</subject><subject>Cerebral hypoxia reperfusion injury</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - metabolism</subject><subject>Hippocampus - pathology</subject><subject>Interleukin-1beta - metabolism</subject><subject>Interleukin-6 - metabolism</subject><subject>Lipid Peroxidation - drug effects</subject><subject>Male</subject><subject>Malondialdehyde - metabolism</subject><subject>Nitric Oxide - metabolism</subject><subject>Peroxidase - metabolism</subject><subject>Rats, Wistar</subject><subject>Reperfusion Injury - drug therapy</subject><subject>Reperfusion Injury - metabolism</subject><subject>Reperfusion Injury - pathology</subject><subject>Stroke</subject><subject>Sulfasalazine</subject><subject>Sulfasalazine - therapeutic use</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><issn>0188-4409</issn><issn>1873-5487</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kF1LwzAUhoMobk7_gUgvvWlNmjRNbwQZ0w0Gwtx9SNJTltIvk1WYv96WbrdenYvzvOflPAg9EhwRTPhLGSlnasijGJM0wjzCmF2hOREpDRMm0ms0x0SIkDGczdCd9yXGWDCe3qJZLLKY0pjP0XpVFGCOPmiL4KuvuoPyqlK_toHANsESHGinqmDjzQFqq4IddOCK3tu2CTZN2bvTyO3U8R7dFKry8HCeC7R_X-2X63D7-bFZvm1DQ3l8DLmIOQAwTSE3ACkInaQp0bHKC9A6SbASXKQMKGGZMklCVZ7TgmrNM1CULtDzdLZz7XcP_ihr6w1UlWqg7b0kGcNJJgglA8om1LjWeweF7JytlTtJguWoUJZyUihHhRJzOSgcYk_nhl6Pu0vo4mwAXicAhjd_LDjpjYXGQG7doFLmrf2_4Q9yyISl</recordid><startdate>201704</startdate><enddate>201704</enddate><creator>Cetin, Cansel</creator><creator>Erdogan, Ahmet Melih</creator><creator>Dincel, Gungor Cagdas</creator><creator>Bakar, Bulent</creator><creator>Kisa, Ucler</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>7X8</scope></search><sort><creationdate>201704</creationdate><title>Effects of Sulphasalazine in Cerebral Ischemia Reperfusion Injury in Rat</title><author>Cetin, Cansel ; Erdogan, Ahmet Melih ; Dincel, Gungor Cagdas ; Bakar, Bulent ; Kisa, Ucler</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c362t-6826eee4b3edcee7e8b5771b2adfebb550a86874e3149ac553add3f3bb69ea33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animals</topic><topic>Anti-Inflammatory Agents, Non-Steroidal - therapeutic use</topic><topic>Antiinflamatory</topic><topic>Brain Edema - drug therapy</topic><topic>Brain Edema - metabolism</topic><topic>Brain Ischemia - drug therapy</topic><topic>Brain Ischemia - metabolism</topic><topic>Brain Ischemia - pathology</topic><topic>Cerebral Cortex - drug effects</topic><topic>Cerebral Cortex - metabolism</topic><topic>Cerebral Cortex - pathology</topic><topic>Cerebral hypoxia reperfusion injury</topic><topic>Hippocampus - drug effects</topic><topic>Hippocampus - metabolism</topic><topic>Hippocampus - pathology</topic><topic>Interleukin-1beta - metabolism</topic><topic>Interleukin-6 - metabolism</topic><topic>Lipid Peroxidation - drug effects</topic><topic>Male</topic><topic>Malondialdehyde - metabolism</topic><topic>Nitric Oxide - metabolism</topic><topic>Peroxidase - metabolism</topic><topic>Rats, Wistar</topic><topic>Reperfusion Injury - drug therapy</topic><topic>Reperfusion Injury - metabolism</topic><topic>Reperfusion Injury - pathology</topic><topic>Stroke</topic><topic>Sulfasalazine</topic><topic>Sulfasalazine - therapeutic use</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cetin, Cansel</creatorcontrib><creatorcontrib>Erdogan, Ahmet Melih</creatorcontrib><creatorcontrib>Dincel, Gungor Cagdas</creatorcontrib><creatorcontrib>Bakar, Bulent</creatorcontrib><creatorcontrib>Kisa, Ucler</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>Archives of medical research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cetin, Cansel</au><au>Erdogan, Ahmet Melih</au><au>Dincel, Gungor Cagdas</au><au>Bakar, Bulent</au><au>Kisa, Ucler</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of Sulphasalazine in Cerebral Ischemia Reperfusion Injury in Rat</atitle><jtitle>Archives of medical research</jtitle><addtitle>Arch Med Res</addtitle><date>2017-04</date><risdate>2017</risdate><volume>48</volume><issue>3</issue><spage>247</spage><epage>256</epage><pages>247-256</pages><issn>0188-4409</issn><eissn>1873-5487</eissn><abstract>Management of cerebral ischemia/reperfusion (I/R) injury is still difficult process today.
Aim of present study was to investigate therapeutic properties of sulfasalazine in cerebral transient I/R injury in rat.
Except Control group (n = 5), 20 Wistar albino rats were allocated for acute and chronic stage investigation of I/R injury, and temporary aneurysm clips were attempted to both internal carotid arteries for thirty min. Four hours later, 40 mg/kg once a day sulfasalazine was administered to animals of SL-A and SL-C groups, orally. Animals were decapitated, following which pyknotic and necrotic neuronal cells, perivascular edema, irregularities of intercellular organization (IIO) of hippocampal regions, and cortical necrotic neurons of parietal lobe were counted or scaled histopathologically. Tissue malonyldialdehyde (MDA), myeloperoxidation (MPO), total nitrite/nitrate (NO), interleukin 1-beta (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) level values were evaluated biochemically.
Sulfasalazine could reduce perivascular edema, IIO, cortical and hippocampal neuronal cell death in both stages. It could decrease MDA in acute stage, but not reduce IL-1β, IL-6, MPO, NO, and TNFα levels. It could increase IL-1β levels in chronic stage but not affect to IL-6, MPO, MDA, NO, TNF-α levels.
Sulfasalazine could improve histopathological architecture of hypoxic tissue in both stages of I/R injury in rat. It could inhibit lipid peroxidation cascades just in acute stage. These results suggested that therapeutic mechanisms of sulfasalazine in cerebral I/R injury should be investigated by using more specific laboratory methods in future studies.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>28923326</pmid><doi>10.1016/j.arcmed.2017.06.004</doi><tpages>10</tpages></addata></record> |
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| subjects | Animals Anti-Inflammatory Agents, Non-Steroidal - therapeutic use Antiinflamatory Brain Edema - drug therapy Brain Edema - metabolism Brain Ischemia - drug therapy Brain Ischemia - metabolism Brain Ischemia - pathology Cerebral Cortex - drug effects Cerebral Cortex - metabolism Cerebral Cortex - pathology Cerebral hypoxia reperfusion injury Hippocampus - drug effects Hippocampus - metabolism Hippocampus - pathology Interleukin-1beta - metabolism Interleukin-6 - metabolism Lipid Peroxidation - drug effects Male Malondialdehyde - metabolism Nitric Oxide - metabolism Peroxidase - metabolism Rats, Wistar Reperfusion Injury - drug therapy Reperfusion Injury - metabolism Reperfusion Injury - pathology Stroke Sulfasalazine Sulfasalazine - therapeutic use Tumor Necrosis Factor-alpha - metabolism |
| title | Effects of Sulphasalazine in Cerebral Ischemia Reperfusion Injury in Rat |
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