Up-Regulation of Advanced Glycated Products Receptors in the Brain of Diabetic Rats Is Prevented by Antioxidant Treatment
Diabetics have at least twice the risk of stroke and may show performance deficit in a wide range of cognitive domains. The mechanisms underlying this gradually developing end-organ damage may involve both vascular changes and direct damage to neuronal cells as a result of overproduction of superoxi...
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| Veröffentlicht in: | Endocrinology (Philadelphia) 2005-12, Vol.146 (12), p.5561-5567 |
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| creator | Aragno, Manuela Mastrocola, Raffaella Medana, Claudio Restivo, Francesca Catalano, Maria G Pons, Nicoletta Danni, Oliviero Boccuzzi, Giuseppe |
| description | Diabetics have at least twice the risk of stroke and may show performance deficit in a wide range of cognitive domains. The mechanisms underlying this gradually developing end-organ damage may involve both vascular changes and direct damage to neuronal cells as a result of overproduction of superoxide by the respiratory chain and consequent oxidative stress. The study aimed to assess the role of oxidative stress on the aldose reductase-polyol pathway, on advanced glycated end-product (AGE)/AGE-receptor interaction, and on downstream signaling in the hippocampus of streptozotocin-treated rats. Data show that, in diabetic rats, levels of prooxidant compounds increase, whereas levels of antioxidant compounds fall. Receptor for AGE and galectin-3 content and polyol flux increase, whereas glyceraldehyde-3-phosphate dehydrogenase activity is impaired. Moreover, nuclear factor κB (p65) transcription factor levels and S-100 protein are increased in the hippocampus cytosol, suggesting that oxidative stress triggers the cascade of events that finally leads to neuronal damage. Dehydroepiandrosterone, the most abundant hormonal steroid in the blood, has been reported to possess antioxidant properties. When dehydroepiandrosterone was administered to diabetic rats, the improved oxidative imbalance and the marked reduction of AGE receptors paralleled the reduced activation of nuclear factor κB and the reduction of S-100 levels, reinforcing the suggestion that oxidative stress plays a role in diabetes-related neuronal damage. |
| doi_str_mv | 10.1210/en.2005-0712 |
| format | Article |
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The mechanisms underlying this gradually developing end-organ damage may involve both vascular changes and direct damage to neuronal cells as a result of overproduction of superoxide by the respiratory chain and consequent oxidative stress. The study aimed to assess the role of oxidative stress on the aldose reductase-polyol pathway, on advanced glycated end-product (AGE)/AGE-receptor interaction, and on downstream signaling in the hippocampus of streptozotocin-treated rats. Data show that, in diabetic rats, levels of prooxidant compounds increase, whereas levels of antioxidant compounds fall. Receptor for AGE and galectin-3 content and polyol flux increase, whereas glyceraldehyde-3-phosphate dehydrogenase activity is impaired. Moreover, nuclear factor κB (p65) transcription factor levels and S-100 protein are increased in the hippocampus cytosol, suggesting that oxidative stress triggers the cascade of events that finally leads to neuronal damage. Dehydroepiandrosterone, the most abundant hormonal steroid in the blood, has been reported to possess antioxidant properties. When dehydroepiandrosterone was administered to diabetic rats, the improved oxidative imbalance and the marked reduction of AGE receptors paralleled the reduced activation of nuclear factor κB and the reduction of S-100 levels, reinforcing the suggestion that oxidative stress plays a role in diabetes-related neuronal damage.</description><identifier>ISSN: 0013-7227</identifier><identifier>EISSN: 1945-7170</identifier><identifier>DOI: 10.1210/en.2005-0712</identifier><identifier>PMID: 16166220</identifier><identifier>CODEN: ENDOAO</identifier><language>eng</language><publisher>Bethesda, MD: Endocrine Society</publisher><subject>Advanced glycosylation end products ; Age ; Aldehyde reductase ; Aldehyde Reductase - metabolism ; Animals ; Antioxidants ; Antioxidants - pharmacology ; Biological and medical sciences ; Brain - metabolism ; Brain damage ; Brain injury ; Cytosol ; Damage assessment ; Damage prevention ; Dehydroepiandrosterone ; Diabetes ; Diabetes mellitus ; Diabetes Mellitus, Experimental - metabolism ; Diabetes. Impaired glucose tolerance ; Electron transport ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Fundamental and applied biological sciences. Psychology ; Galectin-3 ; Glycation End Products, Advanced - metabolism ; Glyceraldehyde-3-phosphate dehydrogenase ; Health risks ; Hippocampus ; Hippocampus - metabolism ; Male ; Medical sciences ; Nerve Growth Factors - metabolism ; NF-kappa B - metabolism ; Oxidative Stress ; Rats ; Rats, Wistar ; Receptor for Advanced Glycation End Products ; Receptor mechanisms ; Receptors ; Receptors, Immunologic - metabolism ; Reductases ; Respiration ; S100 Calcium Binding Protein beta Subunit ; S100 protein ; S100 Proteins - metabolism ; Streptozocin ; Up-Regulation - drug effects ; Vertebrates: endocrinology</subject><ispartof>Endocrinology (Philadelphia), 2005-12, Vol.146 (12), p.5561-5567</ispartof><rights>Copyright © 2005 by The Endocrine Society 2005</rights><rights>2006 INIST-CNRS</rights><rights>Copyright © 2005 by The Endocrine Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c558t-d95d4a3bb79bec0b71790a13f05b55c01e3974e709ff08dc6a5b5c8ab2992aba3</citedby><cites>FETCH-LOGICAL-c558t-d95d4a3bb79bec0b71790a13f05b55c01e3974e709ff08dc6a5b5c8ab2992aba3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17278353$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16166220$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Aragno, Manuela</creatorcontrib><creatorcontrib>Mastrocola, Raffaella</creatorcontrib><creatorcontrib>Medana, Claudio</creatorcontrib><creatorcontrib>Restivo, Francesca</creatorcontrib><creatorcontrib>Catalano, Maria G</creatorcontrib><creatorcontrib>Pons, Nicoletta</creatorcontrib><creatorcontrib>Danni, Oliviero</creatorcontrib><creatorcontrib>Boccuzzi, Giuseppe</creatorcontrib><title>Up-Regulation of Advanced Glycated Products Receptors in the Brain of Diabetic Rats Is Prevented by Antioxidant Treatment</title><title>Endocrinology (Philadelphia)</title><addtitle>Endocrinology</addtitle><description>Diabetics have at least twice the risk of stroke and may show performance deficit in a wide range of cognitive domains. The mechanisms underlying this gradually developing end-organ damage may involve both vascular changes and direct damage to neuronal cells as a result of overproduction of superoxide by the respiratory chain and consequent oxidative stress. The study aimed to assess the role of oxidative stress on the aldose reductase-polyol pathway, on advanced glycated end-product (AGE)/AGE-receptor interaction, and on downstream signaling in the hippocampus of streptozotocin-treated rats. Data show that, in diabetic rats, levels of prooxidant compounds increase, whereas levels of antioxidant compounds fall. Receptor for AGE and galectin-3 content and polyol flux increase, whereas glyceraldehyde-3-phosphate dehydrogenase activity is impaired. Moreover, nuclear factor κB (p65) transcription factor levels and S-100 protein are increased in the hippocampus cytosol, suggesting that oxidative stress triggers the cascade of events that finally leads to neuronal damage. Dehydroepiandrosterone, the most abundant hormonal steroid in the blood, has been reported to possess antioxidant properties. When dehydroepiandrosterone was administered to diabetic rats, the improved oxidative imbalance and the marked reduction of AGE receptors paralleled the reduced activation of nuclear factor κB and the reduction of S-100 levels, reinforcing the suggestion that oxidative stress plays a role in diabetes-related neuronal damage.</description><subject>Advanced glycosylation end products</subject><subject>Age</subject><subject>Aldehyde reductase</subject><subject>Aldehyde Reductase - metabolism</subject><subject>Animals</subject><subject>Antioxidants</subject><subject>Antioxidants - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Brain - metabolism</subject><subject>Brain damage</subject><subject>Brain injury</subject><subject>Cytosol</subject><subject>Damage assessment</subject><subject>Damage prevention</subject><subject>Dehydroepiandrosterone</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus, Experimental - metabolism</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Electron transport</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Galectin-3</subject><subject>Glycation End Products, Advanced - metabolism</subject><subject>Glyceraldehyde-3-phosphate dehydrogenase</subject><subject>Health risks</subject><subject>Hippocampus</subject><subject>Hippocampus - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Nerve Growth Factors - metabolism</subject><subject>NF-kappa B - metabolism</subject><subject>Oxidative Stress</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptor for Advanced Glycation End Products</subject><subject>Receptor mechanisms</subject><subject>Receptors</subject><subject>Receptors, Immunologic - metabolism</subject><subject>Reductases</subject><subject>Respiration</subject><subject>S100 Calcium Binding Protein beta Subunit</subject><subject>S100 protein</subject><subject>S100 Proteins - metabolism</subject><subject>Streptozocin</subject><subject>Up-Regulation - drug effects</subject><subject>Vertebrates: endocrinology</subject><issn>0013-7227</issn><issn>1945-7170</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0c-L1DAUB_Agijuu3jxLQHQvds2PpmmO47quCwvKsHsuSfqqWTpJTdLF-e_NOIUBUTw1bT7vvT6-CL2k5JwySt6DP2eEiIpIyh6hFVW1qCSV5DFaEUJ5JRmTJ-hZSvflta5r_hSd0IY2DWNkhXZ3U7WBb_OoswsehwGv-wftLfT4atxZncvhawz9bHPCG7Aw5RATdh7n74A_RO1-F3102kB2Fm90cdep1MAD-H212eG1L81_ul77jG8j6LwtV8_Rk0GPCV4sz1N09-ny9uJzdfPl6vpifVNZIdpc9Ur0tebGSGXAElNWU0RTPhBhhLCEAleyBknUMJC2t40u322rDVOKaaP5KXp76DvF8GOGlLutSxbGUXsIc-qaVqq2IeS_kCouJa9Fga__gPdhjr4s0XHKiZCijC7q3UHZGFKKMHRTdFsddx0l3T65Dny3T67bJ1f4q6XpbLbQH_ESVQFvFqCT1eMQS0ouHZ1ksuWCF3d2cGGe_jWyWkbygwTfBxudhylCSsdt_vqjvwC2x712</recordid><startdate>20051201</startdate><enddate>20051201</enddate><creator>Aragno, Manuela</creator><creator>Mastrocola, Raffaella</creator><creator>Medana, Claudio</creator><creator>Restivo, Francesca</creator><creator>Catalano, Maria G</creator><creator>Pons, Nicoletta</creator><creator>Danni, Oliviero</creator><creator>Boccuzzi, Giuseppe</creator><general>Endocrine Society</general><general>Oxford University Press</general><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>7QG</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>7TK</scope><scope>7X8</scope></search><sort><creationdate>20051201</creationdate><title>Up-Regulation of Advanced Glycated Products Receptors in the Brain of Diabetic Rats Is Prevented by Antioxidant Treatment</title><author>Aragno, Manuela ; Mastrocola, Raffaella ; Medana, Claudio ; Restivo, Francesca ; Catalano, Maria G ; Pons, Nicoletta ; Danni, Oliviero ; Boccuzzi, Giuseppe</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c558t-d95d4a3bb79bec0b71790a13f05b55c01e3974e709ff08dc6a5b5c8ab2992aba3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Advanced glycosylation end products</topic><topic>Age</topic><topic>Aldehyde reductase</topic><topic>Aldehyde Reductase - metabolism</topic><topic>Animals</topic><topic>Antioxidants</topic><topic>Antioxidants - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Brain - metabolism</topic><topic>Brain damage</topic><topic>Brain injury</topic><topic>Cytosol</topic><topic>Damage assessment</topic><topic>Damage prevention</topic><topic>Dehydroepiandrosterone</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes Mellitus, Experimental - metabolism</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Electron transport</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Galectin-3</topic><topic>Glycation End Products, Advanced - metabolism</topic><topic>Glyceraldehyde-3-phosphate dehydrogenase</topic><topic>Health risks</topic><topic>Hippocampus</topic><topic>Hippocampus - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Nerve Growth Factors - metabolism</topic><topic>NF-kappa B - metabolism</topic><topic>Oxidative Stress</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptor for Advanced Glycation End Products</topic><topic>Receptor mechanisms</topic><topic>Receptors</topic><topic>Receptors, Immunologic - metabolism</topic><topic>Reductases</topic><topic>Respiration</topic><topic>S100 Calcium Binding Protein beta Subunit</topic><topic>S100 protein</topic><topic>S100 Proteins - metabolism</topic><topic>Streptozocin</topic><topic>Up-Regulation - drug effects</topic><topic>Vertebrates: endocrinology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Aragno, Manuela</creatorcontrib><creatorcontrib>Mastrocola, Raffaella</creatorcontrib><creatorcontrib>Medana, Claudio</creatorcontrib><creatorcontrib>Restivo, Francesca</creatorcontrib><creatorcontrib>Catalano, Maria G</creatorcontrib><creatorcontrib>Pons, Nicoletta</creatorcontrib><creatorcontrib>Danni, Oliviero</creatorcontrib><creatorcontrib>Boccuzzi, Giuseppe</creatorcontrib><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>Animal Behavior Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Endocrinology (Philadelphia)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Aragno, Manuela</au><au>Mastrocola, Raffaella</au><au>Medana, Claudio</au><au>Restivo, Francesca</au><au>Catalano, Maria G</au><au>Pons, Nicoletta</au><au>Danni, Oliviero</au><au>Boccuzzi, Giuseppe</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Up-Regulation of Advanced Glycated Products Receptors in the Brain of Diabetic Rats Is Prevented by Antioxidant Treatment</atitle><jtitle>Endocrinology (Philadelphia)</jtitle><addtitle>Endocrinology</addtitle><date>2005-12-01</date><risdate>2005</risdate><volume>146</volume><issue>12</issue><spage>5561</spage><epage>5567</epage><pages>5561-5567</pages><issn>0013-7227</issn><eissn>1945-7170</eissn><coden>ENDOAO</coden><abstract>Diabetics have at least twice the risk of stroke and may show performance deficit in a wide range of cognitive domains. The mechanisms underlying this gradually developing end-organ damage may involve both vascular changes and direct damage to neuronal cells as a result of overproduction of superoxide by the respiratory chain and consequent oxidative stress. The study aimed to assess the role of oxidative stress on the aldose reductase-polyol pathway, on advanced glycated end-product (AGE)/AGE-receptor interaction, and on downstream signaling in the hippocampus of streptozotocin-treated rats. Data show that, in diabetic rats, levels of prooxidant compounds increase, whereas levels of antioxidant compounds fall. Receptor for AGE and galectin-3 content and polyol flux increase, whereas glyceraldehyde-3-phosphate dehydrogenase activity is impaired. Moreover, nuclear factor κB (p65) transcription factor levels and S-100 protein are increased in the hippocampus cytosol, suggesting that oxidative stress triggers the cascade of events that finally leads to neuronal damage. Dehydroepiandrosterone, the most abundant hormonal steroid in the blood, has been reported to possess antioxidant properties. When dehydroepiandrosterone was administered to diabetic rats, the improved oxidative imbalance and the marked reduction of AGE receptors paralleled the reduced activation of nuclear factor κB and the reduction of S-100 levels, reinforcing the suggestion that oxidative stress plays a role in diabetes-related neuronal damage.</abstract><cop>Bethesda, MD</cop><pub>Endocrine Society</pub><pmid>16166220</pmid><doi>10.1210/en.2005-0712</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Advanced glycosylation end products Age Aldehyde reductase Aldehyde Reductase - metabolism Animals Antioxidants Antioxidants - pharmacology Biological and medical sciences Brain - metabolism Brain damage Brain injury Cytosol Damage assessment Damage prevention Dehydroepiandrosterone Diabetes Diabetes mellitus Diabetes Mellitus, Experimental - metabolism Diabetes. Impaired glucose tolerance Electron transport Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Fundamental and applied biological sciences. Psychology Galectin-3 Glycation End Products, Advanced - metabolism Glyceraldehyde-3-phosphate dehydrogenase Health risks Hippocampus Hippocampus - metabolism Male Medical sciences Nerve Growth Factors - metabolism NF-kappa B - metabolism Oxidative Stress Rats Rats, Wistar Receptor for Advanced Glycation End Products Receptor mechanisms Receptors Receptors, Immunologic - metabolism Reductases Respiration S100 Calcium Binding Protein beta Subunit S100 protein S100 Proteins - metabolism Streptozocin Up-Regulation - drug effects Vertebrates: endocrinology |
| title | Up-Regulation of Advanced Glycated Products Receptors in the Brain of Diabetic Rats Is Prevented by Antioxidant Treatment |
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