Tempol alleviates intracerebral hemorrhage-induced brain injury possibly by attenuating nitrative stress
Intracerebral hemorrhage (ICH)-induced brain injury leads to irreversible disruption of the blood–brain barrier (BBB) and fatality brain edema with massive cell death. Although secondary damage could, in principle, be preventable, no effective treatment approaches currently exist for patients with I...
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| Veröffentlicht in: | Neuroreport 2015-09, Vol.26 (14), p.842-849 |
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| creator | Wanyong, Yang Zefeng, Tan Xiufeng, Xin Dawei, Dong Xiaoyan, Liu Ying, Zhao Yaogao, Fu |
| description | Intracerebral hemorrhage (ICH)-induced brain injury leads to irreversible disruption of the blood–brain barrier (BBB) and fatality brain edema with massive cell death. Although secondary damage could, in principle, be preventable, no effective treatment approaches currently exist for patients with ICH. Tempol, a catalytic scavenger of peroxynitrite (ONOO)-derived free radicals, has been proven to ameliorate brain injury in several types of brain insults. This study aims to investigate the potential neuroprotective effect of tempol after ICH and to explore the underlying mechanisms. Collagenase-induced ICH was performed in rats. Tempol was administered immediately after ICH. The effects of tempol on ICH were evaluated by assessing neurological deficits, BBB permeability, brain edema, and apoptotic cell death. The mechanisms of action of tempol, with its clear ability on the derivative of ONOO [3-nitrotyrosine (3-NT), ONOO, and its derivative-mediated nitration marker] and expression of tight junction protein [zonula occludens-1 (ZO-1)], were also investigated. Perihematomal 3-NT increased significantly following ICH and expressed around vessels accompanied by reduced and discontinuous expression of ZO-1. Tempol treatment significantly suppressed 3-NT formation and preserved ZO-1 levels, and led to improvement in neurological outcomes and reduction of BBB leakiness, brain edema, and apoptosis. In conclusion, tempol has neuroprotective potential in experimental ICH and may help combat ICH-induced brain injury in patients. |
| doi_str_mv | 10.1097/WNR.0000000000000434 |
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Although secondary damage could, in principle, be preventable, no effective treatment approaches currently exist for patients with ICH. Tempol, a catalytic scavenger of peroxynitrite (ONOO)-derived free radicals, has been proven to ameliorate brain injury in several types of brain insults. This study aims to investigate the potential neuroprotective effect of tempol after ICH and to explore the underlying mechanisms. Collagenase-induced ICH was performed in rats. Tempol was administered immediately after ICH. The effects of tempol on ICH were evaluated by assessing neurological deficits, BBB permeability, brain edema, and apoptotic cell death. The mechanisms of action of tempol, with its clear ability on the derivative of ONOO [3-nitrotyrosine (3-NT), ONOO, and its derivative-mediated nitration marker] and expression of tight junction protein [zonula occludens-1 (ZO-1)], were also investigated. Perihematomal 3-NT increased significantly following ICH and expressed around vessels accompanied by reduced and discontinuous expression of ZO-1. Tempol treatment significantly suppressed 3-NT formation and preserved ZO-1 levels, and led to improvement in neurological outcomes and reduction of BBB leakiness, brain edema, and apoptosis. In conclusion, tempol has neuroprotective potential in experimental ICH and may help combat ICH-induced brain injury in patients.</description><identifier>ISSN: 0959-4965</identifier><identifier>EISSN: 1473-558X</identifier><identifier>DOI: 10.1097/WNR.0000000000000434</identifier><identifier>PMID: 26237245</identifier><language>eng</language><publisher>England: Wolters Kluwer Health | Lippincott Williams & Wilkins</publisher><subject>Animals ; Antioxidants - pharmacology ; Apoptosis - drug effects ; Apoptosis - physiology ; Blood-Brain Barrier - drug effects ; Blood-Brain Barrier - metabolism ; Blood-Brain Barrier - pathology ; Brain - drug effects ; Brain - pathology ; Brain - physiopathology ; Brain Edema - drug therapy ; Brain Edema - etiology ; Brain Edema - pathology ; Brain Edema - physiopathology ; Brain Injuries - drug therapy ; Brain Injuries - etiology ; Brain Injuries - pathology ; Brain Injuries - physiopathology ; Cerebral Hemorrhage - complications ; Cerebral Hemorrhage - drug therapy ; Cerebral Hemorrhage - pathology ; Cerebral Hemorrhage - physiopathology ; Collagenases ; Cyclic N-Oxides - pharmacology ; Disease Models, Animal ; Male ; Neuroprotective Agents - pharmacology ; Random Allocation ; Rats, Sprague-Dawley ; Spin Labels ; Tyrosine - analogs & derivatives ; Tyrosine - metabolism ; Zonula Occludens-1 Protein - metabolism</subject><ispartof>Neuroreport, 2015-09, Vol.26 (14), p.842-849</ispartof><rights>2015 Wolters Kluwer Health | Lippincott Williams & Wilkins</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3894-af20265da2e00b3b540265461641090686a90228077bd34c1414b6ef60286e3f3</citedby><cites>FETCH-LOGICAL-c3894-af20265da2e00b3b540265461641090686a90228077bd34c1414b6ef60286e3f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27929,27930</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26237245$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wanyong, Yang</creatorcontrib><creatorcontrib>Zefeng, Tan</creatorcontrib><creatorcontrib>Xiufeng, Xin</creatorcontrib><creatorcontrib>Dawei, Dong</creatorcontrib><creatorcontrib>Xiaoyan, Liu</creatorcontrib><creatorcontrib>Ying, Zhao</creatorcontrib><creatorcontrib>Yaogao, Fu</creatorcontrib><title>Tempol alleviates intracerebral hemorrhage-induced brain injury possibly by attenuating nitrative stress</title><title>Neuroreport</title><addtitle>Neuroreport</addtitle><description>Intracerebral hemorrhage (ICH)-induced brain injury leads to irreversible disruption of the blood–brain barrier (BBB) and fatality brain edema with massive cell death. Although secondary damage could, in principle, be preventable, no effective treatment approaches currently exist for patients with ICH. Tempol, a catalytic scavenger of peroxynitrite (ONOO)-derived free radicals, has been proven to ameliorate brain injury in several types of brain insults. This study aims to investigate the potential neuroprotective effect of tempol after ICH and to explore the underlying mechanisms. Collagenase-induced ICH was performed in rats. Tempol was administered immediately after ICH. The effects of tempol on ICH were evaluated by assessing neurological deficits, BBB permeability, brain edema, and apoptotic cell death. The mechanisms of action of tempol, with its clear ability on the derivative of ONOO [3-nitrotyrosine (3-NT), ONOO, and its derivative-mediated nitration marker] and expression of tight junction protein [zonula occludens-1 (ZO-1)], were also investigated. Perihematomal 3-NT increased significantly following ICH and expressed around vessels accompanied by reduced and discontinuous expression of ZO-1. Tempol treatment significantly suppressed 3-NT formation and preserved ZO-1 levels, and led to improvement in neurological outcomes and reduction of BBB leakiness, brain edema, and apoptosis. In conclusion, tempol has neuroprotective potential in experimental ICH and may help combat ICH-induced brain injury in patients.</description><subject>Animals</subject><subject>Antioxidants - pharmacology</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - physiology</subject><subject>Blood-Brain Barrier - drug effects</subject><subject>Blood-Brain Barrier - metabolism</subject><subject>Blood-Brain Barrier - pathology</subject><subject>Brain - drug effects</subject><subject>Brain - pathology</subject><subject>Brain - physiopathology</subject><subject>Brain Edema - drug therapy</subject><subject>Brain Edema - etiology</subject><subject>Brain Edema - pathology</subject><subject>Brain Edema - physiopathology</subject><subject>Brain Injuries - drug therapy</subject><subject>Brain Injuries - etiology</subject><subject>Brain Injuries - pathology</subject><subject>Brain Injuries - physiopathology</subject><subject>Cerebral Hemorrhage - complications</subject><subject>Cerebral Hemorrhage - drug therapy</subject><subject>Cerebral Hemorrhage - pathology</subject><subject>Cerebral Hemorrhage - physiopathology</subject><subject>Collagenases</subject><subject>Cyclic N-Oxides - pharmacology</subject><subject>Disease Models, Animal</subject><subject>Male</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Random Allocation</subject><subject>Rats, Sprague-Dawley</subject><subject>Spin Labels</subject><subject>Tyrosine - analogs & derivatives</subject><subject>Tyrosine - metabolism</subject><subject>Zonula Occludens-1 Protein - metabolism</subject><issn>0959-4965</issn><issn>1473-558X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkctKxTAQhoMoery8gUiWbqpJmqTJUsQbiIIouitpO7XRtD0mqXLe3shRERfibIYZvvmHmR-hXUoOKNHF4f3VzQH5GTznK2hGeZFnQqiHVTQjWuiMayk20GYIT4nRhKp1tMEkywvGxQx1t9DPR4eNc_BqTYSA7RC9qcFD5Y3DHfSj9515hMwOzVRDg1PfDgl7mvwCz8cQbOUWuFpgEyMMk4l2eMSDTSrRvgIO0UMI22itNS7AzmfeQnenJ7fH59nl9dnF8dFlVudK88y0jDApGsOAkCqvBP8ouaSSp6uJVNJowpgiRVE1Oa8pp7yS0ErClIS8zbfQ_lJ37seXCUIsextqcM4MME6hpIVUolBEqX-gpBBCK60Typdo7dO9Htpy7m1v_KKkpPywo0x2lL_tSGN7nxumqofme-jr_wlQS-BtdBF8eHbTG_iyA-Ni97f2OxuVlyw</recordid><startdate>20150930</startdate><enddate>20150930</enddate><creator>Wanyong, Yang</creator><creator>Zefeng, Tan</creator><creator>Xiufeng, Xin</creator><creator>Dawei, Dong</creator><creator>Xiaoyan, Liu</creator><creator>Ying, Zhao</creator><creator>Yaogao, Fu</creator><general>Wolters Kluwer Health | Lippincott Williams & Wilkins</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><scope>7TK</scope></search><sort><creationdate>20150930</creationdate><title>Tempol alleviates intracerebral hemorrhage-induced brain injury possibly by attenuating nitrative stress</title><author>Wanyong, Yang ; Zefeng, Tan ; Xiufeng, Xin ; Dawei, Dong ; Xiaoyan, Liu ; Ying, Zhao ; Yaogao, Fu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3894-af20265da2e00b3b540265461641090686a90228077bd34c1414b6ef60286e3f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Antioxidants - pharmacology</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - physiology</topic><topic>Blood-Brain Barrier - drug effects</topic><topic>Blood-Brain Barrier - metabolism</topic><topic>Blood-Brain Barrier - pathology</topic><topic>Brain - drug effects</topic><topic>Brain - pathology</topic><topic>Brain - physiopathology</topic><topic>Brain Edema - drug therapy</topic><topic>Brain Edema - etiology</topic><topic>Brain Edema - pathology</topic><topic>Brain Edema - physiopathology</topic><topic>Brain Injuries - drug therapy</topic><topic>Brain Injuries - etiology</topic><topic>Brain Injuries - pathology</topic><topic>Brain Injuries - physiopathology</topic><topic>Cerebral Hemorrhage - complications</topic><topic>Cerebral Hemorrhage - drug therapy</topic><topic>Cerebral Hemorrhage - pathology</topic><topic>Cerebral Hemorrhage - physiopathology</topic><topic>Collagenases</topic><topic>Cyclic N-Oxides - pharmacology</topic><topic>Disease Models, Animal</topic><topic>Male</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Random Allocation</topic><topic>Rats, Sprague-Dawley</topic><topic>Spin Labels</topic><topic>Tyrosine - analogs & derivatives</topic><topic>Tyrosine - metabolism</topic><topic>Zonula Occludens-1 Protein - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wanyong, Yang</creatorcontrib><creatorcontrib>Zefeng, Tan</creatorcontrib><creatorcontrib>Xiufeng, Xin</creatorcontrib><creatorcontrib>Dawei, Dong</creatorcontrib><creatorcontrib>Xiaoyan, Liu</creatorcontrib><creatorcontrib>Ying, Zhao</creatorcontrib><creatorcontrib>Yaogao, Fu</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><collection>Neurosciences Abstracts</collection><jtitle>Neuroreport</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wanyong, Yang</au><au>Zefeng, Tan</au><au>Xiufeng, Xin</au><au>Dawei, Dong</au><au>Xiaoyan, Liu</au><au>Ying, Zhao</au><au>Yaogao, Fu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tempol alleviates intracerebral hemorrhage-induced brain injury possibly by attenuating nitrative stress</atitle><jtitle>Neuroreport</jtitle><addtitle>Neuroreport</addtitle><date>2015-09-30</date><risdate>2015</risdate><volume>26</volume><issue>14</issue><spage>842</spage><epage>849</epage><pages>842-849</pages><issn>0959-4965</issn><eissn>1473-558X</eissn><abstract>Intracerebral hemorrhage (ICH)-induced brain injury leads to irreversible disruption of the blood–brain barrier (BBB) and fatality brain edema with massive cell death. Although secondary damage could, in principle, be preventable, no effective treatment approaches currently exist for patients with ICH. Tempol, a catalytic scavenger of peroxynitrite (ONOO)-derived free radicals, has been proven to ameliorate brain injury in several types of brain insults. This study aims to investigate the potential neuroprotective effect of tempol after ICH and to explore the underlying mechanisms. Collagenase-induced ICH was performed in rats. Tempol was administered immediately after ICH. The effects of tempol on ICH were evaluated by assessing neurological deficits, BBB permeability, brain edema, and apoptotic cell death. The mechanisms of action of tempol, with its clear ability on the derivative of ONOO [3-nitrotyrosine (3-NT), ONOO, and its derivative-mediated nitration marker] and expression of tight junction protein [zonula occludens-1 (ZO-1)], were also investigated. Perihematomal 3-NT increased significantly following ICH and expressed around vessels accompanied by reduced and discontinuous expression of ZO-1. Tempol treatment significantly suppressed 3-NT formation and preserved ZO-1 levels, and led to improvement in neurological outcomes and reduction of BBB leakiness, brain edema, and apoptosis. In conclusion, tempol has neuroprotective potential in experimental ICH and may help combat ICH-induced brain injury in patients.</abstract><cop>England</cop><pub>Wolters Kluwer Health | Lippincott Williams & Wilkins</pub><pmid>26237245</pmid><doi>10.1097/WNR.0000000000000434</doi><tpages>8</tpages></addata></record> |
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| subjects | Animals Antioxidants - pharmacology Apoptosis - drug effects Apoptosis - physiology Blood-Brain Barrier - drug effects Blood-Brain Barrier - metabolism Blood-Brain Barrier - pathology Brain - drug effects Brain - pathology Brain - physiopathology Brain Edema - drug therapy Brain Edema - etiology Brain Edema - pathology Brain Edema - physiopathology Brain Injuries - drug therapy Brain Injuries - etiology Brain Injuries - pathology Brain Injuries - physiopathology Cerebral Hemorrhage - complications Cerebral Hemorrhage - drug therapy Cerebral Hemorrhage - pathology Cerebral Hemorrhage - physiopathology Collagenases Cyclic N-Oxides - pharmacology Disease Models, Animal Male Neuroprotective Agents - pharmacology Random Allocation Rats, Sprague-Dawley Spin Labels Tyrosine - analogs & derivatives Tyrosine - metabolism Zonula Occludens-1 Protein - metabolism |
| title | Tempol alleviates intracerebral hemorrhage-induced brain injury possibly by attenuating nitrative stress |
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