Expressions of Inducible Nitric Oxide Synthase and Cyclooxygenase-2 in Gastric Ischemia-Reperfusion: Role of Angiotensin II
Background Angiotensin II contributes to the pathogenesis of inflammation induced by ischemia-reperfusion (I/R) in various organs. Angiotensin II increases vascular permeability that initiates the inflammatory process and leads to the migration of inflammatory cells into the tissue. The aim of the p...
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| Veröffentlicht in: | The Journal of surgical research 2010-06, Vol.161 (1), p.126-133 |
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| description | Background Angiotensin II contributes to the pathogenesis of inflammation induced by ischemia-reperfusion (I/R) in various organs. Angiotensin II increases vascular permeability that initiates the inflammatory process and leads to the migration of inflammatory cells into the tissue. The aim of the present study was to investigate the effect of angiotensin II on ischemia-reperfusion induced expressions of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) in rat stomachs exposed to ischemia-reperfusion. Methods Wistar rats were randomly separated into five groups: sham operated, I/R, I/R plus candesartan (an AT1 receptor antagonist), I/R plus PD123319 (an AT2 receptor antagonist), and I/R plus captopril (an angiotensin-converting enzyme inhibitor). Candesartan (1mg/kg/d), PD123319 (3mg/kg/d), and captopril (20mg/kg/d) were given subcutaneously twice a day for 5 d before I/R. The rats were submitted to gastric ischemia by clamping the celiac artery for 30min followed by 24h reperfusion. Results Candesartan decreased the neutrophil accumulation, iNOS expression, and increased NOx level, COX-2 expression in the gastric tissue exposed to I/R compared with I/R group. PD123319 did not change the neutrophil accumulation, iNOS expression, PGE2 , or NOx levels, but increased the expression of COX-2 in the gastric tissue exposed to I/R. However, captopril did not play any role in I/R induced change in gastric mucosa. Conclusions The results suggest that Angiotensin II via angiotensin II type 1 receptor increases the accumulation of neutrophils and iNOS expression and plays a significant role in mediating inflammation in gastric mucosa exposed to I/R. |
| doi_str_mv | 10.1016/j.jss.2009.07.018 |
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Angiotensin II increases vascular permeability that initiates the inflammatory process and leads to the migration of inflammatory cells into the tissue. The aim of the present study was to investigate the effect of angiotensin II on ischemia-reperfusion induced expressions of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) in rat stomachs exposed to ischemia-reperfusion. Methods Wistar rats were randomly separated into five groups: sham operated, I/R, I/R plus candesartan (an AT1 receptor antagonist), I/R plus PD123319 (an AT2 receptor antagonist), and I/R plus captopril (an angiotensin-converting enzyme inhibitor). Candesartan (1mg/kg/d), PD123319 (3mg/kg/d), and captopril (20mg/kg/d) were given subcutaneously twice a day for 5 d before I/R. The rats were submitted to gastric ischemia by clamping the celiac artery for 30min followed by 24h reperfusion. Results Candesartan decreased the neutrophil accumulation, iNOS expression, and increased NOx level, COX-2 expression in the gastric tissue exposed to I/R compared with I/R group. PD123319 did not change the neutrophil accumulation, iNOS expression, PGE2 , or NOx levels, but increased the expression of COX-2 in the gastric tissue exposed to I/R. However, captopril did not play any role in I/R induced change in gastric mucosa. Conclusions The results suggest that Angiotensin II via angiotensin II type 1 receptor increases the accumulation of neutrophils and iNOS expression and plays a significant role in mediating inflammation in gastric mucosa exposed to I/R.</description><identifier>ISSN: 0022-4804</identifier><identifier>EISSN: 1095-8673</identifier><identifier>DOI: 10.1016/j.jss.2009.07.018</identifier><identifier>PMID: 19959193</identifier><identifier>CODEN: JSGRA2</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>angiotensin II ; Angiotensin II - blood ; Angiotensin II Type 1 Receptor Blockers - pharmacology ; Angiotensin II Type 2 Receptor Blockers ; Angiotensin-Converting Enzyme Inhibitors - pharmacology ; Animals ; Benzimidazoles - pharmacology ; Biological and medical sciences ; candesartan ; captopril ; Captopril - pharmacology ; Cardiology. Vascular system ; COX-2 ; Cyclooxygenase 2 - metabolism ; Dinoprostone - metabolism ; Gastritis - enzymology ; Gastritis - etiology ; General aspects ; Imidazoles - pharmacology ; iNOS ; ischemia-reperfusion ; Male ; Medical sciences ; Neutrophils - metabolism ; Nitric Oxide - metabolism ; Nitric Oxide Synthase Type II - metabolism ; PD123319 ; Peroxidase - metabolism ; Pyridines - pharmacology ; Rats ; Rats, Wistar ; Reperfusion Injury - complications ; Reperfusion Injury - enzymology ; Surgery ; Tetrazoles - pharmacology</subject><ispartof>The Journal of surgical research, 2010-06, Vol.161 (1), p.126-133</ispartof><rights>Elsevier Inc.</rights><rights>2010 Elsevier Inc.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright (c) 2010 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c437t-e5fe6962f130ee40d23318698411908295aa9913e27711c91399bc7f2508891c3</citedby><cites>FETCH-LOGICAL-c437t-e5fe6962f130ee40d23318698411908295aa9913e27711c91399bc7f2508891c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.jss.2009.07.018$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,781,785,3551,27929,27930,46000</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22774099$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19959193$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gemici, Burcu, Ph.D</creatorcontrib><creatorcontrib>Tan, Ruken, Ph.D</creatorcontrib><creatorcontrib>Öngüt, Gözde, M.D</creatorcontrib><creatorcontrib>Nimet İzgüt-Uysal, V., Ph.D</creatorcontrib><title>Expressions of Inducible Nitric Oxide Synthase and Cyclooxygenase-2 in Gastric Ischemia-Reperfusion: Role of Angiotensin II</title><title>The Journal of surgical research</title><addtitle>J Surg Res</addtitle><description>Background Angiotensin II contributes to the pathogenesis of inflammation induced by ischemia-reperfusion (I/R) in various organs. Angiotensin II increases vascular permeability that initiates the inflammatory process and leads to the migration of inflammatory cells into the tissue. The aim of the present study was to investigate the effect of angiotensin II on ischemia-reperfusion induced expressions of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) in rat stomachs exposed to ischemia-reperfusion. Methods Wistar rats were randomly separated into five groups: sham operated, I/R, I/R plus candesartan (an AT1 receptor antagonist), I/R plus PD123319 (an AT2 receptor antagonist), and I/R plus captopril (an angiotensin-converting enzyme inhibitor). Candesartan (1mg/kg/d), PD123319 (3mg/kg/d), and captopril (20mg/kg/d) were given subcutaneously twice a day for 5 d before I/R. The rats were submitted to gastric ischemia by clamping the celiac artery for 30min followed by 24h reperfusion. Results Candesartan decreased the neutrophil accumulation, iNOS expression, and increased NOx level, COX-2 expression in the gastric tissue exposed to I/R compared with I/R group. PD123319 did not change the neutrophil accumulation, iNOS expression, PGE2 , or NOx levels, but increased the expression of COX-2 in the gastric tissue exposed to I/R. However, captopril did not play any role in I/R induced change in gastric mucosa. Conclusions The results suggest that Angiotensin II via angiotensin II type 1 receptor increases the accumulation of neutrophils and iNOS expression and plays a significant role in mediating inflammation in gastric mucosa exposed to I/R.</description><subject>angiotensin II</subject><subject>Angiotensin II - blood</subject><subject>Angiotensin II Type 1 Receptor Blockers - pharmacology</subject><subject>Angiotensin II Type 2 Receptor Blockers</subject><subject>Angiotensin-Converting Enzyme Inhibitors - pharmacology</subject><subject>Animals</subject><subject>Benzimidazoles - pharmacology</subject><subject>Biological and medical sciences</subject><subject>candesartan</subject><subject>captopril</subject><subject>Captopril - pharmacology</subject><subject>Cardiology. Vascular system</subject><subject>COX-2</subject><subject>Cyclooxygenase 2 - metabolism</subject><subject>Dinoprostone - metabolism</subject><subject>Gastritis - enzymology</subject><subject>Gastritis - etiology</subject><subject>General aspects</subject><subject>Imidazoles - pharmacology</subject><subject>iNOS</subject><subject>ischemia-reperfusion</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Neutrophils - metabolism</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide Synthase Type II - metabolism</subject><subject>PD123319</subject><subject>Peroxidase - metabolism</subject><subject>Pyridines - pharmacology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Reperfusion Injury - complications</subject><subject>Reperfusion Injury - enzymology</subject><subject>Surgery</subject><subject>Tetrazoles - pharmacology</subject><issn>0022-4804</issn><issn>1095-8673</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kl2L1DAUhoso7rj6A7yR3ohXrSdJv6IgLMO6Diwu7Op1yKSnu6mdZMxpZYp_3tQZFLzwKh8875vDQ5LkJYOcAave9nlPlHMAmUOdA2seJSsGssyaqhaPkxUA51nRQHGWPCPqIZ5lLZ4mZ0zKUjIpVsnPy8M-IJH1jlLfpRvXTsZuB0w_2zFYk94cbIvp3ezGB02Yatem69kM3h_me3TxKuOpdemVpt_4hswD7qzObnGPoZuW4nfprY-Fsf3C3Vs_oqOY2GyeJ086PRC-OK3nydePl1_Wn7Lrm6vN-uI6M4WoxwzLDitZ8Y4JQCyg5UKwppJNwZiEhstSaymZQF7XjJm4k3Jr6o6X0DSSGXGevDn27oP_PiGNamfJ4DBoh34iVQsRSSGqSLIjaYInCtipfbA7HWbFQC3KVa-icrUoV1CrqDxmXp3ap-0O27-Jk-MIvD4BmoweuqCdsfSH43HsAqSM3Psjh9HFD4tBkbHoDLY2oBlV6-1_x_jwT9oM1tn44DeckXo_BRclK6aIK1B3y99YvgZIANHIRvwCEESyrQ</recordid><startdate>20100601</startdate><enddate>20100601</enddate><creator>Gemici, Burcu, Ph.D</creator><creator>Tan, Ruken, Ph.D</creator><creator>Öngüt, Gözde, M.D</creator><creator>Nimet İzgüt-Uysal, V., Ph.D</creator><general>Elsevier Inc</general><general>Elsevier</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>7X8</scope></search><sort><creationdate>20100601</creationdate><title>Expressions of Inducible Nitric Oxide Synthase and Cyclooxygenase-2 in Gastric Ischemia-Reperfusion: Role of Angiotensin II</title><author>Gemici, Burcu, Ph.D ; Tan, Ruken, Ph.D ; Öngüt, Gözde, M.D ; Nimet İzgüt-Uysal, V., Ph.D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c437t-e5fe6962f130ee40d23318698411908295aa9913e27711c91399bc7f2508891c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>angiotensin II</topic><topic>Angiotensin II - blood</topic><topic>Angiotensin II Type 1 Receptor Blockers - pharmacology</topic><topic>Angiotensin II Type 2 Receptor Blockers</topic><topic>Angiotensin-Converting Enzyme Inhibitors - pharmacology</topic><topic>Animals</topic><topic>Benzimidazoles - pharmacology</topic><topic>Biological and medical sciences</topic><topic>candesartan</topic><topic>captopril</topic><topic>Captopril - pharmacology</topic><topic>Cardiology. Vascular system</topic><topic>COX-2</topic><topic>Cyclooxygenase 2 - metabolism</topic><topic>Dinoprostone - metabolism</topic><topic>Gastritis - enzymology</topic><topic>Gastritis - etiology</topic><topic>General aspects</topic><topic>Imidazoles - pharmacology</topic><topic>iNOS</topic><topic>ischemia-reperfusion</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Neutrophils - metabolism</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide Synthase Type II - metabolism</topic><topic>PD123319</topic><topic>Peroxidase - metabolism</topic><topic>Pyridines - pharmacology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Reperfusion Injury - complications</topic><topic>Reperfusion Injury - enzymology</topic><topic>Surgery</topic><topic>Tetrazoles - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gemici, Burcu, Ph.D</creatorcontrib><creatorcontrib>Tan, Ruken, Ph.D</creatorcontrib><creatorcontrib>Öngüt, Gözde, M.D</creatorcontrib><creatorcontrib>Nimet İzgüt-Uysal, V., Ph.D</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>MEDLINE - Academic</collection><jtitle>The Journal of surgical research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gemici, Burcu, Ph.D</au><au>Tan, Ruken, Ph.D</au><au>Öngüt, Gözde, M.D</au><au>Nimet İzgüt-Uysal, V., Ph.D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Expressions of Inducible Nitric Oxide Synthase and Cyclooxygenase-2 in Gastric Ischemia-Reperfusion: Role of Angiotensin II</atitle><jtitle>The Journal of surgical research</jtitle><addtitle>J Surg Res</addtitle><date>2010-06-01</date><risdate>2010</risdate><volume>161</volume><issue>1</issue><spage>126</spage><epage>133</epage><pages>126-133</pages><issn>0022-4804</issn><eissn>1095-8673</eissn><coden>JSGRA2</coden><abstract>Background Angiotensin II contributes to the pathogenesis of inflammation induced by ischemia-reperfusion (I/R) in various organs. Angiotensin II increases vascular permeability that initiates the inflammatory process and leads to the migration of inflammatory cells into the tissue. The aim of the present study was to investigate the effect of angiotensin II on ischemia-reperfusion induced expressions of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) in rat stomachs exposed to ischemia-reperfusion. Methods Wistar rats were randomly separated into five groups: sham operated, I/R, I/R plus candesartan (an AT1 receptor antagonist), I/R plus PD123319 (an AT2 receptor antagonist), and I/R plus captopril (an angiotensin-converting enzyme inhibitor). Candesartan (1mg/kg/d), PD123319 (3mg/kg/d), and captopril (20mg/kg/d) were given subcutaneously twice a day for 5 d before I/R. The rats were submitted to gastric ischemia by clamping the celiac artery for 30min followed by 24h reperfusion. Results Candesartan decreased the neutrophil accumulation, iNOS expression, and increased NOx level, COX-2 expression in the gastric tissue exposed to I/R compared with I/R group. PD123319 did not change the neutrophil accumulation, iNOS expression, PGE2 , or NOx levels, but increased the expression of COX-2 in the gastric tissue exposed to I/R. However, captopril did not play any role in I/R induced change in gastric mucosa. Conclusions The results suggest that Angiotensin II via angiotensin II type 1 receptor increases the accumulation of neutrophils and iNOS expression and plays a significant role in mediating inflammation in gastric mucosa exposed to I/R.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>19959193</pmid><doi>10.1016/j.jss.2009.07.018</doi><tpages>8</tpages></addata></record> |
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| subjects | angiotensin II Angiotensin II - blood Angiotensin II Type 1 Receptor Blockers - pharmacology Angiotensin II Type 2 Receptor Blockers Angiotensin-Converting Enzyme Inhibitors - pharmacology Animals Benzimidazoles - pharmacology Biological and medical sciences candesartan captopril Captopril - pharmacology Cardiology. Vascular system COX-2 Cyclooxygenase 2 - metabolism Dinoprostone - metabolism Gastritis - enzymology Gastritis - etiology General aspects Imidazoles - pharmacology iNOS ischemia-reperfusion Male Medical sciences Neutrophils - metabolism Nitric Oxide - metabolism Nitric Oxide Synthase Type II - metabolism PD123319 Peroxidase - metabolism Pyridines - pharmacology Rats Rats, Wistar Reperfusion Injury - complications Reperfusion Injury - enzymology Surgery Tetrazoles - pharmacology |
| title | Expressions of Inducible Nitric Oxide Synthase and Cyclooxygenase-2 in Gastric Ischemia-Reperfusion: Role of Angiotensin II |
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