Ramipril protects from free radical induced white matter damage in chronic hypoperfusion in the rat
Abstract We investigated whether the angiotensin converting enzyme inhibitor, ramipril, could attenuate white matter lesions caused by chronic hypoperfusion in the rat, and whether suppression of oxidative stress is involved in the resulting neuroprotection. The ramipril treatment group showed signi...
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| Veröffentlicht in: | Journal of clinical neuroscience 2008-02, Vol.15 (2), p.174-178 |
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| container_title | Journal of clinical neuroscience |
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| creator | Kim, Joong-Seok Yun, Injin Choi, Young Bin Lee, Kwang-Soo Kim, Yeong-In |
| description | Abstract We investigated whether the angiotensin converting enzyme inhibitor, ramipril, could attenuate white matter lesions caused by chronic hypoperfusion in the rat, and whether suppression of oxidative stress is involved in the resulting neuroprotection. The ramipril treatment group showed significant protection from development of white matter lesions in the optic tract, the anterior commissure, the corpus callosum, the internal capsule and the caudoputamen. The level of malondialdehyde (MDA) and the oxidized glutathione (GSSG)/total glutathione (GSHt ) ratio was also significantly decreased in the ramipril group compared to the vehicle-treated group. These results suggest that ramipril can protect against white matter lesions that result from chronic ischemia due to its effects on free radical scavenging. Further efficacy should be studied in the treatment of cerebrovascular insufficiency states and vascular dementia. |
| doi_str_mv | 10.1016/j.jocn.2006.12.003 |
| format | Article |
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The ramipril treatment group showed significant protection from development of white matter lesions in the optic tract, the anterior commissure, the corpus callosum, the internal capsule and the caudoputamen. The level of malondialdehyde (MDA) and the oxidized glutathione (GSSG)/total glutathione (GSHt ) ratio was also significantly decreased in the ramipril group compared to the vehicle-treated group. These results suggest that ramipril can protect against white matter lesions that result from chronic ischemia due to its effects on free radical scavenging. Further efficacy should be studied in the treatment of cerebrovascular insufficiency states and vascular dementia.</description><identifier>ISSN: 0967-5868</identifier><identifier>EISSN: 1532-2653</identifier><identifier>DOI: 10.1016/j.jocn.2006.12.003</identifier><identifier>PMID: 17997315</identifier><language>eng</language><publisher>Scotland: Elsevier Ltd</publisher><subject>Angiotensin-Converting Enzyme Inhibitors - therapeutic use ; Animals ; Brain Injuries - etiology ; Brain Injuries - pathology ; Brain Injuries - prevention & control ; Brain Ischemia - complications ; Chronic cerebral hypoperfusion ; Chronic Disease ; Disease Models, Animal ; Free radical ; Free Radicals - metabolism ; Glutathione - metabolism ; Glutathione Disulfide - metabolism ; Malondialdehyde - metabolism ; Neuroglia - drug effects ; Neuroglia - pathology ; Neurology ; Ramipril ; Ramipril - therapeutic use ; Rat ; Rats ; Rats, Sprague-Dawley ; Scavenger</subject><ispartof>Journal of clinical neuroscience, 2008-02, Vol.15 (2), p.174-178</ispartof><rights>Elsevier Ltd</rights><rights>2006 Elsevier Ltd</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c409t-fe3e1cffa98a89447ac76ef04e10a12d61e0e26fe787dd3ac8284787cb16dbdb3</citedby><cites>FETCH-LOGICAL-c409t-fe3e1cffa98a89447ac76ef04e10a12d61e0e26fe787dd3ac8284787cb16dbdb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S096758680600659X$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17997315$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kim, Joong-Seok</creatorcontrib><creatorcontrib>Yun, Injin</creatorcontrib><creatorcontrib>Choi, Young Bin</creatorcontrib><creatorcontrib>Lee, Kwang-Soo</creatorcontrib><creatorcontrib>Kim, Yeong-In</creatorcontrib><title>Ramipril protects from free radical induced white matter damage in chronic hypoperfusion in the rat</title><title>Journal of clinical neuroscience</title><addtitle>J Clin Neurosci</addtitle><description>Abstract We investigated whether the angiotensin converting enzyme inhibitor, ramipril, could attenuate white matter lesions caused by chronic hypoperfusion in the rat, and whether suppression of oxidative stress is involved in the resulting neuroprotection. The ramipril treatment group showed significant protection from development of white matter lesions in the optic tract, the anterior commissure, the corpus callosum, the internal capsule and the caudoputamen. The level of malondialdehyde (MDA) and the oxidized glutathione (GSSG)/total glutathione (GSHt ) ratio was also significantly decreased in the ramipril group compared to the vehicle-treated group. These results suggest that ramipril can protect against white matter lesions that result from chronic ischemia due to its effects on free radical scavenging. Further efficacy should be studied in the treatment of cerebrovascular insufficiency states and vascular dementia.</description><subject>Angiotensin-Converting Enzyme Inhibitors - therapeutic use</subject><subject>Animals</subject><subject>Brain Injuries - etiology</subject><subject>Brain Injuries - pathology</subject><subject>Brain Injuries - prevention & control</subject><subject>Brain Ischemia - complications</subject><subject>Chronic cerebral hypoperfusion</subject><subject>Chronic Disease</subject><subject>Disease Models, Animal</subject><subject>Free radical</subject><subject>Free Radicals - metabolism</subject><subject>Glutathione - metabolism</subject><subject>Glutathione Disulfide - metabolism</subject><subject>Malondialdehyde - metabolism</subject><subject>Neuroglia - drug effects</subject><subject>Neuroglia - pathology</subject><subject>Neurology</subject><subject>Ramipril</subject><subject>Ramipril - therapeutic use</subject><subject>Rat</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Scavenger</subject><issn>0967-5868</issn><issn>1532-2653</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU9r3DAQxUVoaTZpv0AORafe7OqPLVsQCiG0aSFQaBPoTWilUVeObW0kuWW_fWV2odBDLzMD896D-Q1CV5TUlFDxfqiHYOaaESJqympC-Bna0JaziomWv0AbIkVXtb3oz9FFSgMhRDacvELntJOy47TdIPNNT34f_Yj3MWQwOWEXw1QKAI7aeqNH7Ge7GLD4985nwJPOGSK2etI_oeyw2cUwe4N3h33YQ3RL8mFeF3m3ZuTX6KXTY4I3p36JHj99fLj9XN1_vftye3NfmYbIXDngQI1zWva6l03TadMJcKQBSjRlVlAgwISDru-s5dr0rG_KbLZU2K3d8kv07phbTnleIGU1-WRgHPUMYUmqK9Ba2sgiZEehiSGlCE4VApOOB0WJWtGqQa1o1YpWUaYK2mJ6e0pfthPYv5YTyyK4Pgqg3PjLQ1TJeJgLOB8LWGWD_3_-h3_sZvTzyv8JDpCGsMS50FNUpWJQ39fnrr8looS08gf_AzSvoYM</recordid><startdate>20080201</startdate><enddate>20080201</enddate><creator>Kim, Joong-Seok</creator><creator>Yun, Injin</creator><creator>Choi, Young Bin</creator><creator>Lee, Kwang-Soo</creator><creator>Kim, Yeong-In</creator><general>Elsevier Ltd</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>20080201</creationdate><title>Ramipril protects from free radical induced white matter damage in chronic hypoperfusion in the rat</title><author>Kim, Joong-Seok ; Yun, Injin ; Choi, Young Bin ; Lee, Kwang-Soo ; Kim, Yeong-In</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c409t-fe3e1cffa98a89447ac76ef04e10a12d61e0e26fe787dd3ac8284787cb16dbdb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Angiotensin-Converting Enzyme Inhibitors - therapeutic use</topic><topic>Animals</topic><topic>Brain Injuries - etiology</topic><topic>Brain Injuries - pathology</topic><topic>Brain Injuries - prevention & control</topic><topic>Brain Ischemia - complications</topic><topic>Chronic cerebral hypoperfusion</topic><topic>Chronic Disease</topic><topic>Disease Models, Animal</topic><topic>Free radical</topic><topic>Free Radicals - metabolism</topic><topic>Glutathione - metabolism</topic><topic>Glutathione Disulfide - metabolism</topic><topic>Malondialdehyde - metabolism</topic><topic>Neuroglia - drug effects</topic><topic>Neuroglia - pathology</topic><topic>Neurology</topic><topic>Ramipril</topic><topic>Ramipril - therapeutic use</topic><topic>Rat</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Scavenger</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kim, Joong-Seok</creatorcontrib><creatorcontrib>Yun, Injin</creatorcontrib><creatorcontrib>Choi, Young Bin</creatorcontrib><creatorcontrib>Lee, Kwang-Soo</creatorcontrib><creatorcontrib>Kim, Yeong-In</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>Journal of clinical neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kim, Joong-Seok</au><au>Yun, Injin</au><au>Choi, Young Bin</au><au>Lee, Kwang-Soo</au><au>Kim, Yeong-In</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ramipril protects from free radical induced white matter damage in chronic hypoperfusion in the rat</atitle><jtitle>Journal of clinical neuroscience</jtitle><addtitle>J Clin Neurosci</addtitle><date>2008-02-01</date><risdate>2008</risdate><volume>15</volume><issue>2</issue><spage>174</spage><epage>178</epage><pages>174-178</pages><issn>0967-5868</issn><eissn>1532-2653</eissn><abstract>Abstract We investigated whether the angiotensin converting enzyme inhibitor, ramipril, could attenuate white matter lesions caused by chronic hypoperfusion in the rat, and whether suppression of oxidative stress is involved in the resulting neuroprotection. The ramipril treatment group showed significant protection from development of white matter lesions in the optic tract, the anterior commissure, the corpus callosum, the internal capsule and the caudoputamen. The level of malondialdehyde (MDA) and the oxidized glutathione (GSSG)/total glutathione (GSHt ) ratio was also significantly decreased in the ramipril group compared to the vehicle-treated group. These results suggest that ramipril can protect against white matter lesions that result from chronic ischemia due to its effects on free radical scavenging. Further efficacy should be studied in the treatment of cerebrovascular insufficiency states and vascular dementia.</abstract><cop>Scotland</cop><pub>Elsevier Ltd</pub><pmid>17997315</pmid><doi>10.1016/j.jocn.2006.12.003</doi><tpages>5</tpages></addata></record> |
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| ispartof | Journal of clinical neuroscience, 2008-02, Vol.15 (2), p.174-178 |
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| subjects | Angiotensin-Converting Enzyme Inhibitors - therapeutic use Animals Brain Injuries - etiology Brain Injuries - pathology Brain Injuries - prevention & control Brain Ischemia - complications Chronic cerebral hypoperfusion Chronic Disease Disease Models, Animal Free radical Free Radicals - metabolism Glutathione - metabolism Glutathione Disulfide - metabolism Malondialdehyde - metabolism Neuroglia - drug effects Neuroglia - pathology Neurology Ramipril Ramipril - therapeutic use Rat Rats Rats, Sprague-Dawley Scavenger |
| title | Ramipril protects from free radical induced white matter damage in chronic hypoperfusion in the rat |
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