Reduction of ischemic brain injury by administration of palmitoylethanolamide after transient middle cerebral artery occlusion in rats
Abstract Stroke is the third leading cause of death and the leading cause of long-term disability in adults. Current therapeutic strategies for stroke, including thrombolytic drugs, such as tissue plasminogen activator offer great promise for the treatment, but complimentary neuroprotective treatmen...
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| Veröffentlicht in: | Brain research 2012-10, Vol.1477, p.45-58 |
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| creator | Ahmad, Akbar Genovese, Tiziana Impellizzeri, Daniela Crupi, Rosalia Velardi, Enrico Marino, Angela Esposito, Emanuela Cuzzocrea, Salvatore |
| description | Abstract Stroke is the third leading cause of death and the leading cause of long-term disability in adults. Current therapeutic strategies for stroke, including thrombolytic drugs, such as tissue plasminogen activator offer great promise for the treatment, but complimentary neuroprotective treatments are likely to provide a better outcome. To counteract the ischemic brain injury in mice, a new therapeutic approach has been employed by using palmitoylethanolamide (PEA). PEA is one of the members of N-acyl-ethanolamine family maintain not only redox balance but also inhibit the mechanisms of secondary injury on ischemic brain injury. Treatment of the middle cerebral artery occlusion (MCAo)-induced animals with PEA reduced edema and brain infractions as evidenced by decreased 2,3,5-triphenyltetrazolium chloride (TTC) staining across brain sections. PEA-mediated improvements in tissues histology shown by reduction of lesion size and improvement in apoptosis level (assayed by Bax and Bcl-2) further support the efficacy of PEA therapy. We demonstrated that PEA treatment blocked infiltration of astrocytes and restored MCAo-mediated reduced expression of PAR, nitrotyrosine, iNOS, chymase, tryptase, growth factors (BDNF and GDNF) and GFAP. PEA also inhibited the MCAo-mediated increased expression of pJNK, NF-κB, and degradation of IκB-α. PEA-treated injured animals improved neurobehavioral functions as evaluated by motor deficits. Based on these findings we propose that PEA would be useful in lowering the risk of damage or improving function in ischemia–reperfusion brain injury-related disorders. |
| doi_str_mv | 10.1016/j.brainres.2012.08.006 |
| format | Article |
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Current therapeutic strategies for stroke, including thrombolytic drugs, such as tissue plasminogen activator offer great promise for the treatment, but complimentary neuroprotective treatments are likely to provide a better outcome. To counteract the ischemic brain injury in mice, a new therapeutic approach has been employed by using palmitoylethanolamide (PEA). PEA is one of the members of N-acyl-ethanolamine family maintain not only redox balance but also inhibit the mechanisms of secondary injury on ischemic brain injury. Treatment of the middle cerebral artery occlusion (MCAo)-induced animals with PEA reduced edema and brain infractions as evidenced by decreased 2,3,5-triphenyltetrazolium chloride (TTC) staining across brain sections. PEA-mediated improvements in tissues histology shown by reduction of lesion size and improvement in apoptosis level (assayed by Bax and Bcl-2) further support the efficacy of PEA therapy. We demonstrated that PEA treatment blocked infiltration of astrocytes and restored MCAo-mediated reduced expression of PAR, nitrotyrosine, iNOS, chymase, tryptase, growth factors (BDNF and GDNF) and GFAP. PEA also inhibited the MCAo-mediated increased expression of pJNK, NF-κB, and degradation of IκB-α. PEA-treated injured animals improved neurobehavioral functions as evaluated by motor deficits. Based on these findings we propose that PEA would be useful in lowering the risk of damage or improving function in ischemia–reperfusion brain injury-related disorders.</description><identifier>ISSN: 0006-8993</identifier><identifier>EISSN: 1872-6240</identifier><identifier>DOI: 10.1016/j.brainres.2012.08.006</identifier><identifier>PMID: 23046519</identifier><identifier>CODEN: BRREAP</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>2,3,5-triphenyltetrazolium chloride ; adults ; Amides ; Animals ; Apoptosis ; Astrocytes ; Astrocytes - metabolism ; Astrocytes - pathology ; Biological and medical sciences ; brain ; Brain Injuries - drug therapy ; Brain Injuries - etiology ; Brain injury ; Brain-derived neurotrophic factor ; Cerebral blood flow ; Cerebral ischemia ; Chloride ; death ; Disease Models, Animal ; Drugs ; Edema ; Endocannabinoids - administration & dosage ; Ethanolamines - administration & dosage ; Glial cell line-derived neurotrophic factor ; Glial fibrillary acidic protein ; Glial Fibrillary Acidic Protein - metabolism ; growth factors ; histology ; Infarction, Middle Cerebral Artery - complications ; Inflammation ; Ischemia ; JNK Mitogen-Activated Protein Kinases - metabolism ; Male ; Medical sciences ; mice ; Neurology ; Neuronal death ; Neuroprotection ; Neuroprotective Agents - administration & dosage ; NF- Kappa B protein ; NF-kappaB-Inducing Kinase ; Nitric Oxide Synthase Type II - metabolism ; Nitric-oxide synthase ; Nitrotyrosine ; Palmitic Acids - administration & dosage ; palmitoylethanolamide ; Protein Serine-Threonine Kinases - metabolism ; Rats ; Rats, Wistar ; Reperfusion Injury - drug therapy ; risk ; Stroke ; t-plasminogen activator ; Tetrazolium Salts ; therapeutics ; thrombolysis ; Tryptase ; Tumor Necrosis Factor-alpha - metabolism ; Vascular diseases and vascular malformations of the nervous system</subject><ispartof>Brain research, 2012-10, Vol.1477, p.45-58</ispartof><rights>Elsevier B.V.</rights><rights>2012 Elsevier B.V.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2012 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c510t-4395775b95350602a81fbd1da54108badc1d1036bf6e9e231e4baafa7817f3913</citedby><cites>FETCH-LOGICAL-c510t-4395775b95350602a81fbd1da54108badc1d1036bf6e9e231e4baafa7817f3913</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.brainres.2012.08.006$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3548,27923,27924,45994</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26415102$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23046519$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ahmad, Akbar</creatorcontrib><creatorcontrib>Genovese, Tiziana</creatorcontrib><creatorcontrib>Impellizzeri, Daniela</creatorcontrib><creatorcontrib>Crupi, Rosalia</creatorcontrib><creatorcontrib>Velardi, Enrico</creatorcontrib><creatorcontrib>Marino, Angela</creatorcontrib><creatorcontrib>Esposito, Emanuela</creatorcontrib><creatorcontrib>Cuzzocrea, Salvatore</creatorcontrib><title>Reduction of ischemic brain injury by administration of palmitoylethanolamide after transient middle cerebral artery occlusion in rats</title><title>Brain research</title><addtitle>Brain Res</addtitle><description>Abstract Stroke is the third leading cause of death and the leading cause of long-term disability in adults. Current therapeutic strategies for stroke, including thrombolytic drugs, such as tissue plasminogen activator offer great promise for the treatment, but complimentary neuroprotective treatments are likely to provide a better outcome. To counteract the ischemic brain injury in mice, a new therapeutic approach has been employed by using palmitoylethanolamide (PEA). PEA is one of the members of N-acyl-ethanolamine family maintain not only redox balance but also inhibit the mechanisms of secondary injury on ischemic brain injury. Treatment of the middle cerebral artery occlusion (MCAo)-induced animals with PEA reduced edema and brain infractions as evidenced by decreased 2,3,5-triphenyltetrazolium chloride (TTC) staining across brain sections. PEA-mediated improvements in tissues histology shown by reduction of lesion size and improvement in apoptosis level (assayed by Bax and Bcl-2) further support the efficacy of PEA therapy. We demonstrated that PEA treatment blocked infiltration of astrocytes and restored MCAo-mediated reduced expression of PAR, nitrotyrosine, iNOS, chymase, tryptase, growth factors (BDNF and GDNF) and GFAP. PEA also inhibited the MCAo-mediated increased expression of pJNK, NF-κB, and degradation of IκB-α. PEA-treated injured animals improved neurobehavioral functions as evaluated by motor deficits. Based on these findings we propose that PEA would be useful in lowering the risk of damage or improving function in ischemia–reperfusion brain injury-related disorders.</description><subject>2,3,5-triphenyltetrazolium chloride</subject><subject>adults</subject><subject>Amides</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Astrocytes</subject><subject>Astrocytes - metabolism</subject><subject>Astrocytes - pathology</subject><subject>Biological and medical sciences</subject><subject>brain</subject><subject>Brain Injuries - drug therapy</subject><subject>Brain Injuries - etiology</subject><subject>Brain injury</subject><subject>Brain-derived neurotrophic factor</subject><subject>Cerebral blood flow</subject><subject>Cerebral ischemia</subject><subject>Chloride</subject><subject>death</subject><subject>Disease Models, Animal</subject><subject>Drugs</subject><subject>Edema</subject><subject>Endocannabinoids - administration & dosage</subject><subject>Ethanolamines - administration & dosage</subject><subject>Glial cell line-derived neurotrophic factor</subject><subject>Glial fibrillary acidic protein</subject><subject>Glial Fibrillary Acidic Protein - metabolism</subject><subject>growth factors</subject><subject>histology</subject><subject>Infarction, Middle Cerebral Artery - complications</subject><subject>Inflammation</subject><subject>Ischemia</subject><subject>JNK Mitogen-Activated Protein Kinases - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>mice</subject><subject>Neurology</subject><subject>Neuronal death</subject><subject>Neuroprotection</subject><subject>Neuroprotective Agents - administration & dosage</subject><subject>NF- Kappa B protein</subject><subject>NF-kappaB-Inducing Kinase</subject><subject>Nitric Oxide Synthase Type II - metabolism</subject><subject>Nitric-oxide synthase</subject><subject>Nitrotyrosine</subject><subject>Palmitic Acids - administration & dosage</subject><subject>palmitoylethanolamide</subject><subject>Protein Serine-Threonine Kinases - metabolism</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Reperfusion Injury - drug therapy</subject><subject>risk</subject><subject>Stroke</subject><subject>t-plasminogen activator</subject><subject>Tetrazolium Salts</subject><subject>therapeutics</subject><subject>thrombolysis</subject><subject>Tryptase</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Vascular diseases and vascular malformations of the nervous system</subject><issn>0006-8993</issn><issn>1872-6240</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNks9u1DAQxiMEoqXwCsUXJC67eOI4iS8IVPFPqoRE6dly7An14sSLnSDlBXhuJuwuSFzgZHn8m2_G801RXALfAof6xW7bJePHhHlbcii3vN1yXt8rzqFtyk1dVvx-cc4ptGmVEmfFo5x3dBVC8YfFWSl4VUtQ58WPT-hmO_k4stgzn-0dDt6yX-LMj7s5LaxbmHGDH32ekjmhexMGP8Ul4HRnxhjM4B0y00-YGGFj9jhOjIIuILOYkCQDM4neFxatDXNelagKaebHxYPehIxPjudFcfv2zeer95vrj-8-XL2-3lgJfNpUQsmmkZ2SQvKal6aFvnPgjKyAt51xFhxwUXd9jQpLAVh1xvSmaaHphQJxUTw_6O5T_DZjnvRAf8YQzIhxzhq4ki2Ujar-BxWVBJANofUBtSnmnLDX--QHkxaC9GqX3umTXXq1S_NWkzeUeHmsMXcDut9pJ38IeHYETLYm9DRY6_Mfrq6ABlMS9_TA9SZq8yURc3tDlSR5rqqar0qvDgTSeL97TDpbssii8wntpF30_-725V8SNtBWUF9fccG8i3MayTwNOlOOvlnXb90-WEVU04qfX0LXKw</recordid><startdate>20121005</startdate><enddate>20121005</enddate><creator>Ahmad, Akbar</creator><creator>Genovese, Tiziana</creator><creator>Impellizzeri, Daniela</creator><creator>Crupi, Rosalia</creator><creator>Velardi, Enrico</creator><creator>Marino, Angela</creator><creator>Esposito, Emanuela</creator><creator>Cuzzocrea, Salvatore</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>FBQ</scope><scope>IQODW</scope><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></search><sort><creationdate>20121005</creationdate><title>Reduction of ischemic brain injury by administration of palmitoylethanolamide after transient middle cerebral artery occlusion in rats</title><author>Ahmad, Akbar ; Genovese, Tiziana ; Impellizzeri, Daniela ; Crupi, Rosalia ; Velardi, Enrico ; Marino, Angela ; Esposito, Emanuela ; Cuzzocrea, Salvatore</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c510t-4395775b95350602a81fbd1da54108badc1d1036bf6e9e231e4baafa7817f3913</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>2,3,5-triphenyltetrazolium chloride</topic><topic>adults</topic><topic>Amides</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Astrocytes</topic><topic>Astrocytes - metabolism</topic><topic>Astrocytes - pathology</topic><topic>Biological and medical sciences</topic><topic>brain</topic><topic>Brain Injuries - drug therapy</topic><topic>Brain Injuries - etiology</topic><topic>Brain injury</topic><topic>Brain-derived neurotrophic factor</topic><topic>Cerebral blood flow</topic><topic>Cerebral ischemia</topic><topic>Chloride</topic><topic>death</topic><topic>Disease Models, Animal</topic><topic>Drugs</topic><topic>Edema</topic><topic>Endocannabinoids - administration & dosage</topic><topic>Ethanolamines - administration & dosage</topic><topic>Glial cell line-derived neurotrophic factor</topic><topic>Glial fibrillary acidic protein</topic><topic>Glial Fibrillary Acidic Protein - metabolism</topic><topic>growth factors</topic><topic>histology</topic><topic>Infarction, Middle Cerebral Artery - complications</topic><topic>Inflammation</topic><topic>Ischemia</topic><topic>JNK Mitogen-Activated Protein Kinases - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>mice</topic><topic>Neurology</topic><topic>Neuronal death</topic><topic>Neuroprotection</topic><topic>Neuroprotective Agents - administration & dosage</topic><topic>NF- Kappa B protein</topic><topic>NF-kappaB-Inducing Kinase</topic><topic>Nitric Oxide Synthase Type II - metabolism</topic><topic>Nitric-oxide synthase</topic><topic>Nitrotyrosine</topic><topic>Palmitic Acids - administration & dosage</topic><topic>palmitoylethanolamide</topic><topic>Protein Serine-Threonine Kinases - metabolism</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Reperfusion Injury - drug therapy</topic><topic>risk</topic><topic>Stroke</topic><topic>t-plasminogen activator</topic><topic>Tetrazolium Salts</topic><topic>therapeutics</topic><topic>thrombolysis</topic><topic>Tryptase</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ahmad, Akbar</creatorcontrib><creatorcontrib>Genovese, Tiziana</creatorcontrib><creatorcontrib>Impellizzeri, Daniela</creatorcontrib><creatorcontrib>Crupi, Rosalia</creatorcontrib><creatorcontrib>Velardi, Enrico</creatorcontrib><creatorcontrib>Marino, Angela</creatorcontrib><creatorcontrib>Esposito, Emanuela</creatorcontrib><creatorcontrib>Cuzzocrea, Salvatore</creatorcontrib><collection>AGRIS</collection><collection>Pascal-Francis</collection><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><jtitle>Brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ahmad, Akbar</au><au>Genovese, Tiziana</au><au>Impellizzeri, Daniela</au><au>Crupi, Rosalia</au><au>Velardi, Enrico</au><au>Marino, Angela</au><au>Esposito, Emanuela</au><au>Cuzzocrea, Salvatore</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Reduction of ischemic brain injury by administration of palmitoylethanolamide after transient middle cerebral artery occlusion in rats</atitle><jtitle>Brain research</jtitle><addtitle>Brain Res</addtitle><date>2012-10-05</date><risdate>2012</risdate><volume>1477</volume><spage>45</spage><epage>58</epage><pages>45-58</pages><issn>0006-8993</issn><eissn>1872-6240</eissn><coden>BRREAP</coden><abstract>Abstract Stroke is the third leading cause of death and the leading cause of long-term disability in adults. Current therapeutic strategies for stroke, including thrombolytic drugs, such as tissue plasminogen activator offer great promise for the treatment, but complimentary neuroprotective treatments are likely to provide a better outcome. To counteract the ischemic brain injury in mice, a new therapeutic approach has been employed by using palmitoylethanolamide (PEA). PEA is one of the members of N-acyl-ethanolamine family maintain not only redox balance but also inhibit the mechanisms of secondary injury on ischemic brain injury. Treatment of the middle cerebral artery occlusion (MCAo)-induced animals with PEA reduced edema and brain infractions as evidenced by decreased 2,3,5-triphenyltetrazolium chloride (TTC) staining across brain sections. PEA-mediated improvements in tissues histology shown by reduction of lesion size and improvement in apoptosis level (assayed by Bax and Bcl-2) further support the efficacy of PEA therapy. We demonstrated that PEA treatment blocked infiltration of astrocytes and restored MCAo-mediated reduced expression of PAR, nitrotyrosine, iNOS, chymase, tryptase, growth factors (BDNF and GDNF) and GFAP. PEA also inhibited the MCAo-mediated increased expression of pJNK, NF-κB, and degradation of IκB-α. PEA-treated injured animals improved neurobehavioral functions as evaluated by motor deficits. Based on these findings we propose that PEA would be useful in lowering the risk of damage or improving function in ischemia–reperfusion brain injury-related disorders.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>23046519</pmid><doi>10.1016/j.brainres.2012.08.006</doi><tpages>14</tpages></addata></record> |
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| subjects | 2,3,5-triphenyltetrazolium chloride adults Amides Animals Apoptosis Astrocytes Astrocytes - metabolism Astrocytes - pathology Biological and medical sciences brain Brain Injuries - drug therapy Brain Injuries - etiology Brain injury Brain-derived neurotrophic factor Cerebral blood flow Cerebral ischemia Chloride death Disease Models, Animal Drugs Edema Endocannabinoids - administration & dosage Ethanolamines - administration & dosage Glial cell line-derived neurotrophic factor Glial fibrillary acidic protein Glial Fibrillary Acidic Protein - metabolism growth factors histology Infarction, Middle Cerebral Artery - complications Inflammation Ischemia JNK Mitogen-Activated Protein Kinases - metabolism Male Medical sciences mice Neurology Neuronal death Neuroprotection Neuroprotective Agents - administration & dosage NF- Kappa B protein NF-kappaB-Inducing Kinase Nitric Oxide Synthase Type II - metabolism Nitric-oxide synthase Nitrotyrosine Palmitic Acids - administration & dosage palmitoylethanolamide Protein Serine-Threonine Kinases - metabolism Rats Rats, Wistar Reperfusion Injury - drug therapy risk Stroke t-plasminogen activator Tetrazolium Salts therapeutics thrombolysis Tryptase Tumor Necrosis Factor-alpha - metabolism Vascular diseases and vascular malformations of the nervous system |
| title | Reduction of ischemic brain injury by administration of palmitoylethanolamide after transient middle cerebral artery occlusion in rats |
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