Inhibition of Type 1 Diabetic Hyperalgesia in Streptozotocin-Induced Wistar versus Spontaneous Gene-Prone BB/Worchester Rats: Efficacy of a Selective Bradykinin B1 Receptor Antagonist
Insulin-dependent type 1 diabetes (T1D) is linked to a series of complications, including painful diabetic neuropathy (PDN). Several neurovascular systems are activated in T1D, including the inducible bradykinin (BK) B1 receptor (BKB1-R) subtype. We assessed and compared the efficacy profile of a se...
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description | Insulin-dependent type 1 diabetes (T1D) is linked to a series of complications, including painful diabetic neuropathy (PDN). Several neurovascular systems are activated in T1D, including the inducible bradykinin (BK) B1 receptor (BKB1-R) subtype. We assessed and compared the efficacy profile of a selective BKB1-R antagonist on hyperalgesia in 2 models of T1Dstreptozotocin (STZ) chemically induced diabetic Wistar rats and spontaneous BioBreeding/Worchester diabetic-prone (BB/Wor-DP) rats. Nociception was measured using the hot plate test to determine thermal hyperalgesia. STZ diabetic rats developed maximal hyperalgesia (35% decrease in their hot plate reaction time) within a week and remained in such condition and degree for up to 4 weeks postinjection. BB/Wor-DP rats also developed hyperalgesia over time that preceded hyperglycemia, starting at the age of 6 weeks (9% decrease in the hot plate reaction time) and stabilizing over the age of 16 to 24 weeks to a maximum (60% decrease in the hot plate reaction time). Single, acute subcutaneous administration of the selective BKB1-R antagonist induced significant time- and dose-dependent attenuation of hyperalgesia in both STZ diabetic and BB/Wor-DP rats. Thus, selective antagonism of the inducible BKB1-R subtype may constitute a novel and potential therapeutic approach for the treatment of PDN. |
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Several neurovascular systems are activated in T1D, including the inducible bradykinin (BK) B1 receptor (BKB1-R) subtype. We assessed and compared the efficacy profile of a selective BKB1-R antagonist on hyperalgesia in 2 models of T1Dstreptozotocin (STZ) chemically induced diabetic Wistar rats and spontaneous BioBreeding/Worchester diabetic-prone (BB/Wor-DP) rats. Nociception was measured using the hot plate test to determine thermal hyperalgesia. STZ diabetic rats developed maximal hyperalgesia (35% decrease in their hot plate reaction time) within a week and remained in such condition and degree for up to 4 weeks postinjection. BB/Wor-DP rats also developed hyperalgesia over time that preceded hyperglycemia, starting at the age of 6 weeks (9% decrease in the hot plate reaction time) and stabilizing over the age of 16 to 24 weeks to a maximum (60% decrease in the hot plate reaction time). Single, acute subcutaneous administration of the selective BKB1-R antagonist induced significant time- and dose-dependent attenuation of hyperalgesia in both STZ diabetic and BB/Wor-DP rats. Thus, selective antagonism of the inducible BKB1-R subtype may constitute a novel and potential therapeutic approach for the treatment of PDN.</description><identifier>ISSN: 0022-3069</identifier><identifier>EISSN: 1554-6578</identifier><identifier>DOI: 10.1097/01.jnen.0000178448.79713.5f</identifier><identifier>PMID: 16141788</identifier><identifier>CODEN: JNENAD</identifier><language>eng</language><publisher>Hagerstown, MD: American Association of Neuropathologists, Inc</publisher><subject>Animals ; Biological and medical sciences ; Bradykinin - analogs & derivatives ; Bradykinin - pharmacokinetics ; Bradykinin - therapeutic use ; Bradykinin B1 Receptor Antagonists ; Carbohydrates (enzymatic deficiencies). Glycogenosis ; Diabetes Mellitus, Experimental - complications ; Diabetes Mellitus, Experimental - genetics ; Diabetic Neuropathies - drug therapy ; Diseases of striated muscles. Neuromuscular diseases ; Errors of metabolism ; Hot Temperature ; Hyperalgesia - drug therapy ; Hyperalgesia - etiology ; Male ; Medical sciences ; Metabolic diseases ; Neurology ; Pain - drug therapy ; Pain - etiology ; Pain Measurement ; Rats ; Rats, Wistar</subject><ispartof>Journal of neuropathology and experimental neurology, 2005-09, Vol.64 (9), p.782-789</ispartof><rights>2005 American Association of Neuropathologists, Inc</rights><rights>2005 INIST-CNRS</rights><rights>Copyright American Association of Neuropathologists, Inc. Sep 2005</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17111846$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16141788$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gabra, Bichoy H</creatorcontrib><creatorcontrib>Benrezzak, Ouhida</creatorcontrib><creatorcontrib>Pheng, Leng-Hong</creatorcontrib><creatorcontrib>Duta, Dana</creatorcontrib><creatorcontrib>Daull, Philippe</creatorcontrib><creatorcontrib>Sirois, Pierre</creatorcontrib><creatorcontrib>Nantel, François</creatorcontrib><creatorcontrib>Battistini, Bruno</creatorcontrib><title>Inhibition of Type 1 Diabetic Hyperalgesia in Streptozotocin-Induced Wistar versus Spontaneous Gene-Prone BB/Worchester Rats: Efficacy of a Selective Bradykinin B1 Receptor Antagonist</title><title>Journal of neuropathology and experimental neurology</title><addtitle>J Neuropathol Exp Neurol</addtitle><description>Insulin-dependent type 1 diabetes (T1D) is linked to a series of complications, including painful diabetic neuropathy (PDN). Several neurovascular systems are activated in T1D, including the inducible bradykinin (BK) B1 receptor (BKB1-R) subtype. We assessed and compared the efficacy profile of a selective BKB1-R antagonist on hyperalgesia in 2 models of T1Dstreptozotocin (STZ) chemically induced diabetic Wistar rats and spontaneous BioBreeding/Worchester diabetic-prone (BB/Wor-DP) rats. Nociception was measured using the hot plate test to determine thermal hyperalgesia. STZ diabetic rats developed maximal hyperalgesia (35% decrease in their hot plate reaction time) within a week and remained in such condition and degree for up to 4 weeks postinjection. BB/Wor-DP rats also developed hyperalgesia over time that preceded hyperglycemia, starting at the age of 6 weeks (9% decrease in the hot plate reaction time) and stabilizing over the age of 16 to 24 weeks to a maximum (60% decrease in the hot plate reaction time). Single, acute subcutaneous administration of the selective BKB1-R antagonist induced significant time- and dose-dependent attenuation of hyperalgesia in both STZ diabetic and BB/Wor-DP rats. Thus, selective antagonism of the inducible BKB1-R subtype may constitute a novel and potential therapeutic approach for the treatment of PDN.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Bradykinin - analogs & derivatives</subject><subject>Bradykinin - pharmacokinetics</subject><subject>Bradykinin - therapeutic use</subject><subject>Bradykinin B1 Receptor Antagonists</subject><subject>Carbohydrates (enzymatic deficiencies). Glycogenosis</subject><subject>Diabetes Mellitus, Experimental - complications</subject><subject>Diabetes Mellitus, Experimental - genetics</subject><subject>Diabetic Neuropathies - drug therapy</subject><subject>Diseases of striated muscles. Neuromuscular diseases</subject><subject>Errors of metabolism</subject><subject>Hot Temperature</subject><subject>Hyperalgesia - drug therapy</subject><subject>Hyperalgesia - etiology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Metabolic diseases</subject><subject>Neurology</subject><subject>Pain - drug therapy</subject><subject>Pain - etiology</subject><subject>Pain Measurement</subject><subject>Rats</subject><subject>Rats, Wistar</subject><issn>0022-3069</issn><issn>1554-6578</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNpdktFu0zAUhiMEYmXwCsgCwV06O45jm7t1jK3SJNA6tMvIcU5ad6md2c6m8mK8Ho5ahIRvjs_R5_P_x3aWfSR4TrDkZ5jMtxbsHKdFuChLMeeSEzpn3YtsRhgr84px8TKbYVwUOcWVPMnehLBNvMSyfJ2dkIqU6aiYZb-XdmMaE42zyHXobj8AIuirUQ1Eo9F1yr3q1xCMQsaiVfQwRPfLRaeNzZe2HTW06N6EqDx6Ah_GgFaDs1FZcGl_BRbyH95ZQIvF2b3zegMhgke3KoYv6LLrjFZ6P2krtIIedDRPifWq3T8YmyQXBN2CnlQ9Ok99184mtbfZq071Ad4d42n289vl3cV1fvP9anlxfpOvC0aqnAKTwCVtG9pJLVquOCt0yUTZQSO7pqWaVRoqjkE0HBcKRNs1uAEqMW14RU-zz4e-g3ePY7Je70zQ0PeH-epKMEaZLBP44T9w60Zvk7e6KCTHXLAiQe-P0NjsoK0Hb3bK7-u_75GAT0dABa36ziurTfjHcUKIKCdb5YF7dn26zfDQj8_g6w2oPm7q6WcwzIu8mKJMWT6VKvoHmwmvLg</recordid><startdate>200509</startdate><enddate>200509</enddate><creator>Gabra, Bichoy H</creator><creator>Benrezzak, Ouhida</creator><creator>Pheng, Leng-Hong</creator><creator>Duta, Dana</creator><creator>Daull, Philippe</creator><creator>Sirois, Pierre</creator><creator>Nantel, François</creator><creator>Battistini, Bruno</creator><general>American Association of Neuropathologists, Inc</general><general>Lippincott Williams & Wilkins</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>88I</scope><scope>8AF</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>S0X</scope><scope>7X8</scope></search><sort><creationdate>200509</creationdate><title>Inhibition of Type 1 Diabetic Hyperalgesia in Streptozotocin-Induced Wistar versus Spontaneous Gene-Prone BB/Worchester Rats: Efficacy of a Selective Bradykinin B1 Receptor Antagonist</title><author>Gabra, Bichoy H ; Benrezzak, Ouhida ; Pheng, Leng-Hong ; Duta, Dana ; Daull, Philippe ; Sirois, Pierre ; Nantel, François ; Battistini, Bruno</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-g2516-3e59e793db3f9c8d7a752c4584feb9fbd3c56ce670e8b702ae8dfb0be3903b763</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Bradykinin - analogs & derivatives</topic><topic>Bradykinin - pharmacokinetics</topic><topic>Bradykinin - therapeutic use</topic><topic>Bradykinin B1 Receptor Antagonists</topic><topic>Carbohydrates (enzymatic deficiencies). Glycogenosis</topic><topic>Diabetes Mellitus, Experimental - complications</topic><topic>Diabetes Mellitus, Experimental - genetics</topic><topic>Diabetic Neuropathies - drug therapy</topic><topic>Diseases of striated muscles. Neuromuscular diseases</topic><topic>Errors of metabolism</topic><topic>Hot Temperature</topic><topic>Hyperalgesia - drug therapy</topic><topic>Hyperalgesia - etiology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Metabolic diseases</topic><topic>Neurology</topic><topic>Pain - drug therapy</topic><topic>Pain - etiology</topic><topic>Pain Measurement</topic><topic>Rats</topic><topic>Rats, Wistar</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gabra, Bichoy H</creatorcontrib><creatorcontrib>Benrezzak, Ouhida</creatorcontrib><creatorcontrib>Pheng, Leng-Hong</creatorcontrib><creatorcontrib>Duta, Dana</creatorcontrib><creatorcontrib>Daull, Philippe</creatorcontrib><creatorcontrib>Sirois, Pierre</creatorcontrib><creatorcontrib>Nantel, François</creatorcontrib><creatorcontrib>Battistini, Bruno</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>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>SIRS Editorial</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of neuropathology and experimental neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gabra, Bichoy H</au><au>Benrezzak, Ouhida</au><au>Pheng, Leng-Hong</au><au>Duta, Dana</au><au>Daull, Philippe</au><au>Sirois, Pierre</au><au>Nantel, François</au><au>Battistini, Bruno</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of Type 1 Diabetic Hyperalgesia in Streptozotocin-Induced Wistar versus Spontaneous Gene-Prone BB/Worchester Rats: Efficacy of a Selective Bradykinin B1 Receptor Antagonist</atitle><jtitle>Journal of neuropathology and experimental neurology</jtitle><addtitle>J Neuropathol Exp Neurol</addtitle><date>2005-09</date><risdate>2005</risdate><volume>64</volume><issue>9</issue><spage>782</spage><epage>789</epage><pages>782-789</pages><issn>0022-3069</issn><eissn>1554-6578</eissn><coden>JNENAD</coden><abstract>Insulin-dependent type 1 diabetes (T1D) is linked to a series of complications, including painful diabetic neuropathy (PDN). Several neurovascular systems are activated in T1D, including the inducible bradykinin (BK) B1 receptor (BKB1-R) subtype. We assessed and compared the efficacy profile of a selective BKB1-R antagonist on hyperalgesia in 2 models of T1Dstreptozotocin (STZ) chemically induced diabetic Wistar rats and spontaneous BioBreeding/Worchester diabetic-prone (BB/Wor-DP) rats. Nociception was measured using the hot plate test to determine thermal hyperalgesia. STZ diabetic rats developed maximal hyperalgesia (35% decrease in their hot plate reaction time) within a week and remained in such condition and degree for up to 4 weeks postinjection. BB/Wor-DP rats also developed hyperalgesia over time that preceded hyperglycemia, starting at the age of 6 weeks (9% decrease in the hot plate reaction time) and stabilizing over the age of 16 to 24 weeks to a maximum (60% decrease in the hot plate reaction time). Single, acute subcutaneous administration of the selective BKB1-R antagonist induced significant time- and dose-dependent attenuation of hyperalgesia in both STZ diabetic and BB/Wor-DP rats. Thus, selective antagonism of the inducible BKB1-R subtype may constitute a novel and potential therapeutic approach for the treatment of PDN.</abstract><cop>Hagerstown, MD</cop><pub>American Association of Neuropathologists, Inc</pub><pmid>16141788</pmid><doi>10.1097/01.jnen.0000178448.79713.5f</doi><tpages>8</tpages></addata></record> |
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source | MEDLINE; Journals@Ovid Complete; Oxford University Press Journals All Titles (1996-Current); EZB-FREE-00999 freely available EZB journals |
subjects | Animals Biological and medical sciences Bradykinin - analogs & derivatives Bradykinin - pharmacokinetics Bradykinin - therapeutic use Bradykinin B1 Receptor Antagonists Carbohydrates (enzymatic deficiencies). Glycogenosis Diabetes Mellitus, Experimental - complications Diabetes Mellitus, Experimental - genetics Diabetic Neuropathies - drug therapy Diseases of striated muscles. Neuromuscular diseases Errors of metabolism Hot Temperature Hyperalgesia - drug therapy Hyperalgesia - etiology Male Medical sciences Metabolic diseases Neurology Pain - drug therapy Pain - etiology Pain Measurement Rats Rats, Wistar |
title | Inhibition of Type 1 Diabetic Hyperalgesia in Streptozotocin-Induced Wistar versus Spontaneous Gene-Prone BB/Worchester Rats: Efficacy of a Selective Bradykinin B1 Receptor Antagonist |
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