Renoprotective effects of prazosin on ischemia-reperfusion injury in rats
Background: Renal ischemia-reperfusion (IR) injury is one of the main leading causes of acute kidney injury associated with inflammation, oxidative stress and cell apoptosis. We studied the effects of prazosin, as a specific blocker of α1-AR, on renal IR injury. Methods: Rats were divided into norma...
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| Veröffentlicht in: | Human & experimental toxicology 2021-08, Vol.40 (8), p.1263-1273 |
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| creator | Rahimi, MM Bagheri, A Bagheri, Y Fathi, E Bagheri, S Nia, AV Jafari, S Montazersaheb, S |
| description | Background:
Renal ischemia-reperfusion (IR) injury is one of the main leading causes of acute kidney injury associated with inflammation, oxidative stress and cell apoptosis. We studied the effects of prazosin, as a specific blocker of α1-AR, on renal IR injury.
Methods:
Rats were divided into normal control; untreated IR and prazosin-treated IR (1 mg/kg body weight). Prazosin was administered by intraperitoneal injection 30 min prior to IR induction. The level of urea/creatinine and oxidative factors were detected by colorimetric methods. Apoptosis-associated factors, inflammatory, and signaling proteins were analyzed in renal tissue. The abnormalities of renal histopathology were detected by immunohistochemistry.
Results:
Administration of prazosin to IR rats ameliorated serum urea and creatinine and IR-induced histopathological damages. Lipid peroxidation was significantly improved after treatment by prazosin in IR injury rats, however, antioxidant status was not affected. Rats subjected to IR injury activated Bax protein and NF-κB mediated inflammatory response. Moreover, treatment with prazosin inhibited renal NF-κB activation, resulting in a significant decline in pro-inflammatory cytokine of IL-6.
Conclusion:
These findings suggest that prazosin could be a good candidate to attenuate renal IR injury due to its ability to modulate renal function, apoptosis and inflammation. |
| doi_str_mv | 10.1177/0960327121993224 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_AFRWT</sourceid><recordid>TN_cdi_proquest_journals_2553720165</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sage_id>10.1177_0960327121993224</sage_id><sourcerecordid>2553720165</sourcerecordid><originalsourceid>FETCH-LOGICAL-c407t-64dfaeb8ead6470843d2bd2136b93cf896e4722f624a8ea6279a26f4ab34c7dc3</originalsourceid><addsrcrecordid>eNp1kM1LAzEQxYMotlbvnmTBczTfaY5S_CgUBNHzks1OdIvdrMmuoH-9WVoVBE8zzPzmveEhdErJBaVaXxKjCGeaMmoMZ0zsoSkVWmNiCN9H03GNx_0EHaW0JoQoI-khmnAupZGET9HyAdrQxdCD65t3KMD73KUi-KKL9jOkpi1CWzTJvcCmsThCB9EPqRmH7XqIH7kU0fbpGB14-5rgZFdn6Onm-nFxh1f3t8vF1Qo7QXSPlai9hWoOtlZCk7ngNatqRrmqDHd-bhQIzZhXTNgMKaaNZcoLW3HhdO34DJ1vdfPXbwOkvlyHIbbZsmRScs0IVTJTZEu5GFKK4MsuNhsbP0pKyjG78m92-eRsJzxUG6h_Dr7DygDeAsk-w6_rv4Jfj-F2dw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2553720165</pqid></control><display><type>article</type><title>Renoprotective effects of prazosin on ischemia-reperfusion injury in rats</title><source>SAGE Open Access Journals</source><creator>Rahimi, MM ; Bagheri, A ; Bagheri, Y ; Fathi, E ; Bagheri, S ; Nia, AV ; Jafari, S ; Montazersaheb, S</creator><creatorcontrib>Rahimi, MM ; Bagheri, A ; Bagheri, Y ; Fathi, E ; Bagheri, S ; Nia, AV ; Jafari, S ; Montazersaheb, S</creatorcontrib><description>Background:
Renal ischemia-reperfusion (IR) injury is one of the main leading causes of acute kidney injury associated with inflammation, oxidative stress and cell apoptosis. We studied the effects of prazosin, as a specific blocker of α1-AR, on renal IR injury.
Methods:
Rats were divided into normal control; untreated IR and prazosin-treated IR (1 mg/kg body weight). Prazosin was administered by intraperitoneal injection 30 min prior to IR induction. The level of urea/creatinine and oxidative factors were detected by colorimetric methods. Apoptosis-associated factors, inflammatory, and signaling proteins were analyzed in renal tissue. The abnormalities of renal histopathology were detected by immunohistochemistry.
Results:
Administration of prazosin to IR rats ameliorated serum urea and creatinine and IR-induced histopathological damages. Lipid peroxidation was significantly improved after treatment by prazosin in IR injury rats, however, antioxidant status was not affected. Rats subjected to IR injury activated Bax protein and NF-κB mediated inflammatory response. Moreover, treatment with prazosin inhibited renal NF-κB activation, resulting in a significant decline in pro-inflammatory cytokine of IL-6.
Conclusion:
These findings suggest that prazosin could be a good candidate to attenuate renal IR injury due to its ability to modulate renal function, apoptosis and inflammation.</description><identifier>ISSN: 0960-3271</identifier><identifier>EISSN: 1477-0903</identifier><identifier>DOI: 10.1177/0960327121993224</identifier><identifier>PMID: 33559503</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>Abnormalities ; Acute Kidney Injury - drug therapy ; Acute Kidney Injury - metabolism ; Acute Kidney Injury - pathology ; Animals ; Anti-Inflammatory Agents - pharmacology ; Anti-Inflammatory Agents - therapeutic use ; Antioxidants ; Apoptosis ; Apoptosis - drug effects ; BAX protein ; Body weight ; Colorimetry ; Creatinine ; Cytokines ; Cytokines - metabolism ; Histopathology ; Immunohistochemistry ; Inflammation ; Inflammatory response ; Injuries ; Interleukin 6 ; Ischemia ; Kidney - drug effects ; Kidney - metabolism ; Kidney - pathology ; Lipid peroxidation ; Lipids ; Male ; NF-kappa B - metabolism ; NF-κB protein ; Oxidative stress ; Oxidative Stress - drug effects ; Peroxidation ; Prazosin ; Prazosin - pharmacology ; Prazosin - therapeutic use ; Protective Agents - pharmacology ; Protective Agents - therapeutic use ; Proteins ; Rats ; Rats, Wistar ; Renal function ; Reperfusion ; Reperfusion Injury - drug therapy ; Reperfusion Injury - metabolism ; Reperfusion Injury - pathology ; Signal Transduction - drug effects ; Urea</subject><ispartof>Human & experimental toxicology, 2021-08, Vol.40 (8), p.1263-1273</ispartof><rights>The Author(s) 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c407t-64dfaeb8ead6470843d2bd2136b93cf896e4722f624a8ea6279a26f4ab34c7dc3</citedby><cites>FETCH-LOGICAL-c407t-64dfaeb8ead6470843d2bd2136b93cf896e4722f624a8ea6279a26f4ab34c7dc3</cites><orcidid>0000-0001-5010-7293</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://journals.sagepub.com/doi/pdf/10.1177/0960327121993224$$EPDF$$P50$$Gsage$$H</linktopdf><linktohtml>$$Uhttps://journals.sagepub.com/doi/10.1177/0960327121993224$$EHTML$$P50$$Gsage$$H</linktohtml><link.rule.ids>314,776,780,21945,27830,27901,27902,44921,45309</link.rule.ids><linktorsrc>$$Uhttps://journals.sagepub.com/doi/full/10.1177/0960327121993224?utm_source=summon&utm_medium=discovery-provider$$EView_record_in_SAGE_Publications$$FView_record_in_$$GSAGE_Publications</linktorsrc><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33559503$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rahimi, MM</creatorcontrib><creatorcontrib>Bagheri, A</creatorcontrib><creatorcontrib>Bagheri, Y</creatorcontrib><creatorcontrib>Fathi, E</creatorcontrib><creatorcontrib>Bagheri, S</creatorcontrib><creatorcontrib>Nia, AV</creatorcontrib><creatorcontrib>Jafari, S</creatorcontrib><creatorcontrib>Montazersaheb, S</creatorcontrib><title>Renoprotective effects of prazosin on ischemia-reperfusion injury in rats</title><title>Human & experimental toxicology</title><addtitle>Hum Exp Toxicol</addtitle><description>Background:
Renal ischemia-reperfusion (IR) injury is one of the main leading causes of acute kidney injury associated with inflammation, oxidative stress and cell apoptosis. We studied the effects of prazosin, as a specific blocker of α1-AR, on renal IR injury.
Methods:
Rats were divided into normal control; untreated IR and prazosin-treated IR (1 mg/kg body weight). Prazosin was administered by intraperitoneal injection 30 min prior to IR induction. The level of urea/creatinine and oxidative factors were detected by colorimetric methods. Apoptosis-associated factors, inflammatory, and signaling proteins were analyzed in renal tissue. The abnormalities of renal histopathology were detected by immunohistochemistry.
Results:
Administration of prazosin to IR rats ameliorated serum urea and creatinine and IR-induced histopathological damages. Lipid peroxidation was significantly improved after treatment by prazosin in IR injury rats, however, antioxidant status was not affected. Rats subjected to IR injury activated Bax protein and NF-κB mediated inflammatory response. Moreover, treatment with prazosin inhibited renal NF-κB activation, resulting in a significant decline in pro-inflammatory cytokine of IL-6.
Conclusion:
These findings suggest that prazosin could be a good candidate to attenuate renal IR injury due to its ability to modulate renal function, apoptosis and inflammation.</description><subject>Abnormalities</subject><subject>Acute Kidney Injury - drug therapy</subject><subject>Acute Kidney Injury - metabolism</subject><subject>Acute Kidney Injury - pathology</subject><subject>Animals</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Anti-Inflammatory Agents - therapeutic use</subject><subject>Antioxidants</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>BAX protein</subject><subject>Body weight</subject><subject>Colorimetry</subject><subject>Creatinine</subject><subject>Cytokines</subject><subject>Cytokines - metabolism</subject><subject>Histopathology</subject><subject>Immunohistochemistry</subject><subject>Inflammation</subject><subject>Inflammatory response</subject><subject>Injuries</subject><subject>Interleukin 6</subject><subject>Ischemia</subject><subject>Kidney - drug effects</subject><subject>Kidney - metabolism</subject><subject>Kidney - pathology</subject><subject>Lipid peroxidation</subject><subject>Lipids</subject><subject>Male</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB protein</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Peroxidation</subject><subject>Prazosin</subject><subject>Prazosin - pharmacology</subject><subject>Prazosin - therapeutic use</subject><subject>Protective Agents - pharmacology</subject><subject>Protective Agents - therapeutic use</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Renal function</subject><subject>Reperfusion</subject><subject>Reperfusion Injury - drug therapy</subject><subject>Reperfusion Injury - metabolism</subject><subject>Reperfusion Injury - pathology</subject><subject>Signal Transduction - drug effects</subject><subject>Urea</subject><issn>0960-3271</issn><issn>1477-0903</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kM1LAzEQxYMotlbvnmTBczTfaY5S_CgUBNHzks1OdIvdrMmuoH-9WVoVBE8zzPzmveEhdErJBaVaXxKjCGeaMmoMZ0zsoSkVWmNiCN9H03GNx_0EHaW0JoQoI-khmnAupZGET9HyAdrQxdCD65t3KMD73KUi-KKL9jOkpi1CWzTJvcCmsThCB9EPqRmH7XqIH7kU0fbpGB14-5rgZFdn6Onm-nFxh1f3t8vF1Qo7QXSPlai9hWoOtlZCk7ngNatqRrmqDHd-bhQIzZhXTNgMKaaNZcoLW3HhdO34DJ1vdfPXbwOkvlyHIbbZsmRScs0IVTJTZEu5GFKK4MsuNhsbP0pKyjG78m92-eRsJzxUG6h_Dr7DygDeAsk-w6_rv4Jfj-F2dw</recordid><startdate>202108</startdate><enddate>202108</enddate><creator>Rahimi, MM</creator><creator>Bagheri, A</creator><creator>Bagheri, Y</creator><creator>Fathi, E</creator><creator>Bagheri, S</creator><creator>Nia, AV</creator><creator>Jafari, S</creator><creator>Montazersaheb, S</creator><general>SAGE Publications</general><general>Sage Publications 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>7ST</scope><scope>7TK</scope><scope>7U7</scope><scope>C1K</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>SOI</scope><orcidid>https://orcid.org/0000-0001-5010-7293</orcidid></search><sort><creationdate>202108</creationdate><title>Renoprotective effects of prazosin on ischemia-reperfusion injury in rats</title><author>Rahimi, MM ; Bagheri, A ; Bagheri, Y ; Fathi, E ; Bagheri, S ; Nia, AV ; Jafari, S ; Montazersaheb, S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c407t-64dfaeb8ead6470843d2bd2136b93cf896e4722f624a8ea6279a26f4ab34c7dc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Abnormalities</topic><topic>Acute Kidney Injury - drug therapy</topic><topic>Acute Kidney Injury - metabolism</topic><topic>Acute Kidney Injury - pathology</topic><topic>Animals</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Anti-Inflammatory Agents - therapeutic use</topic><topic>Antioxidants</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>BAX protein</topic><topic>Body weight</topic><topic>Colorimetry</topic><topic>Creatinine</topic><topic>Cytokines</topic><topic>Cytokines - metabolism</topic><topic>Histopathology</topic><topic>Immunohistochemistry</topic><topic>Inflammation</topic><topic>Inflammatory response</topic><topic>Injuries</topic><topic>Interleukin 6</topic><topic>Ischemia</topic><topic>Kidney - drug effects</topic><topic>Kidney - metabolism</topic><topic>Kidney - pathology</topic><topic>Lipid peroxidation</topic><topic>Lipids</topic><topic>Male</topic><topic>NF-kappa B - metabolism</topic><topic>NF-κB protein</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Peroxidation</topic><topic>Prazosin</topic><topic>Prazosin - pharmacology</topic><topic>Prazosin - therapeutic use</topic><topic>Protective Agents - pharmacology</topic><topic>Protective Agents - therapeutic use</topic><topic>Proteins</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Renal function</topic><topic>Reperfusion</topic><topic>Reperfusion Injury - drug therapy</topic><topic>Reperfusion Injury - metabolism</topic><topic>Reperfusion Injury - pathology</topic><topic>Signal Transduction - drug effects</topic><topic>Urea</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rahimi, MM</creatorcontrib><creatorcontrib>Bagheri, A</creatorcontrib><creatorcontrib>Bagheri, Y</creatorcontrib><creatorcontrib>Fathi, E</creatorcontrib><creatorcontrib>Bagheri, S</creatorcontrib><creatorcontrib>Nia, AV</creatorcontrib><creatorcontrib>Jafari, S</creatorcontrib><creatorcontrib>Montazersaheb, S</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Environment Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>Environment Abstracts</collection><jtitle>Human & experimental toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Rahimi, MM</au><au>Bagheri, A</au><au>Bagheri, Y</au><au>Fathi, E</au><au>Bagheri, S</au><au>Nia, AV</au><au>Jafari, S</au><au>Montazersaheb, S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Renoprotective effects of prazosin on ischemia-reperfusion injury in rats</atitle><jtitle>Human & experimental toxicology</jtitle><addtitle>Hum Exp Toxicol</addtitle><date>2021-08</date><risdate>2021</risdate><volume>40</volume><issue>8</issue><spage>1263</spage><epage>1273</epage><pages>1263-1273</pages><issn>0960-3271</issn><eissn>1477-0903</eissn><abstract>Background:
Renal ischemia-reperfusion (IR) injury is one of the main leading causes of acute kidney injury associated with inflammation, oxidative stress and cell apoptosis. We studied the effects of prazosin, as a specific blocker of α1-AR, on renal IR injury.
Methods:
Rats were divided into normal control; untreated IR and prazosin-treated IR (1 mg/kg body weight). Prazosin was administered by intraperitoneal injection 30 min prior to IR induction. The level of urea/creatinine and oxidative factors were detected by colorimetric methods. Apoptosis-associated factors, inflammatory, and signaling proteins were analyzed in renal tissue. The abnormalities of renal histopathology were detected by immunohistochemistry.
Results:
Administration of prazosin to IR rats ameliorated serum urea and creatinine and IR-induced histopathological damages. Lipid peroxidation was significantly improved after treatment by prazosin in IR injury rats, however, antioxidant status was not affected. Rats subjected to IR injury activated Bax protein and NF-κB mediated inflammatory response. Moreover, treatment with prazosin inhibited renal NF-κB activation, resulting in a significant decline in pro-inflammatory cytokine of IL-6.
Conclusion:
These findings suggest that prazosin could be a good candidate to attenuate renal IR injury due to its ability to modulate renal function, apoptosis and inflammation.</abstract><cop>London, England</cop><pub>SAGE Publications</pub><pmid>33559503</pmid><doi>10.1177/0960327121993224</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0001-5010-7293</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Abnormalities Acute Kidney Injury - drug therapy Acute Kidney Injury - metabolism Acute Kidney Injury - pathology Animals Anti-Inflammatory Agents - pharmacology Anti-Inflammatory Agents - therapeutic use Antioxidants Apoptosis Apoptosis - drug effects BAX protein Body weight Colorimetry Creatinine Cytokines Cytokines - metabolism Histopathology Immunohistochemistry Inflammation Inflammatory response Injuries Interleukin 6 Ischemia Kidney - drug effects Kidney - metabolism Kidney - pathology Lipid peroxidation Lipids Male NF-kappa B - metabolism NF-κB protein Oxidative stress Oxidative Stress - drug effects Peroxidation Prazosin Prazosin - pharmacology Prazosin - therapeutic use Protective Agents - pharmacology Protective Agents - therapeutic use Proteins Rats Rats, Wistar Renal function Reperfusion Reperfusion Injury - drug therapy Reperfusion Injury - metabolism Reperfusion Injury - pathology Signal Transduction - drug effects Urea |
| title | Renoprotective effects of prazosin on ischemia-reperfusion injury in rats |
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