Effects of aminoguanidine and melatonin on intestinal ischemia/reperfusion injury in rats: An assessor-blinded, controlled experimental study
Abstract Background: The reactive oxygen and nitrogen species generated during reperfusion of tissue are characteristic of intestinal ischemia and reperfusion (IIR) injury. Objective: This study was designed to assess whether the administration of aminoguanidine (AG), a selective nitric oxide syntha...
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| Veröffentlicht in: | Current therapeutic research 2009-12, Vol.70 (6), p.449-459 |
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| creator | Tunc, Turan, MD Kesik, Vural, MD Demirin, Hilmi, MD Ersoz, Nail, MD Vurucu, Sebahattin, MD Kul, Mustafa, MD Uysal, Bülent, MD Sadir, Serdar, MD Guven, Ahmet, MD Oztas, Emin, MD |
| description | Abstract Background: The reactive oxygen and nitrogen species generated during reperfusion of tissue are characteristic of intestinal ischemia and reperfusion (IIR) injury. Objective: This study was designed to assess whether the administration of aminoguanidine (AG), a selective nitric oxide synthase inhibitor, and/or melatonin has protective potential in IIR injury. Methods: Male Wistar albino rats (age, 3–4 weeks; weight, 100–150 g) were divided in a nonrandom fashion into 5 groups of equal size: group 1, IIR injury + AG 100 mg/kg; group 2, IIR injury + melatonin 10 mg/kg; group 3, IIR injury + AG 100 mg/kg + melatonin 10 mg/kg; group 4, sham operation; and group 5, IIR injury alone. Sixty minutes of intestinal ischemia and 4 hours of reperfusion were carried out in all but the sham-operation group. Ileal specimens were obtained from all rats to determine the extent of histologic changes, measure tissue concentrations of malondialdehyde (MDA) and protein carbonyl (PC), and assess the activity of superoxide dismutase (SOD) and glutathione peroxidase (GPx). Specimens were also assessed and scored by a pathologist blinded to the experiment and the data. Results: Forty rats were divided into 5 groups of 8 each; all 40 survived until study end. In the IIR injury-alone group, mean (SD) MDA concentration and PC content were significantly higher than that of the sham-operation group, and SOD and GPx activity were significantly lower: MDA concentration, 0.86 (0.03) versus 0.54 (0.01) mmol/g protein, respectively; PC content, 0.60 (0.02) versus 0.34 (0.01) mmol/g protein; SOD activity, 104.33 (43.14) versus 2954.72 (109.55) U/g protein; and GPx activity, 10.44 (0.63) versus 24.34 (1.77) U/g protein (all, P < 0.001). Administration of AG, melatonin, and the AG/melatonin combination was associated with significantly higher SOD (1802.31 [102.35], 1776.50 [58.41], and 1924.28 [98.10] U/g protein, respectively) and GPx (17.36 [1.23], 15.96 [1.08], and 18.06 [1.72] U/g protein) activity and significantly lower MDA concentration (0.62 [0.02], 0.64 [0.02], and 0.56 [0.01] mmol/g protein) and PC content (0.53 [0.03], 0.51 [0.01], and 0.49 [0.02] mmol/g protein) compared with the IIR injury-alone group ( P < 0.001). Mean intestinal mucosal injury scores were significantly lower in the 3 treatment groups (2.12 [0.35], 1.75 [0.46], and 1.12 [0.35]) compared with the IIR injury-alone group (3.87 [0.35]; all, P < 0.001). Conclusion: In this study, AG, melatonin, or both admini |
| doi_str_mv | 10.1016/j.curtheres.2009.12.002 |
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| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3969984</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>1_s2_0_S0011393X09001040</els_id><sourcerecordid>1512559847</sourcerecordid><originalsourceid>FETCH-LOGICAL-c560t-b966209c2c2ef11f588293b03c6622be423345a6cd1b17c6a376b21692fa552b3</originalsourceid><addsrcrecordid>eNqNUsmO1DAQjRCIaQZ-AXxB4kAyXjqLOYzUGg2LNBIHQOJmOU5l2k1iN65kRH8E_0w13TTLiVNZrlevXtWrLHsmeCG4qC42hZvTtIYEWEjOdSFkwbm8ly1EU-ucK6HuZwvOhciVVp_PskeIG855xev6YXYml5WWjaoX2ffrvgc3IYs9s6MP8Xa2wXc-ALOhYyMMdorBBxYD82ECnHywA_Po1jB6e5FgC6mf0f_Mb-a0o8CSnfAVWwVmEQExprwdfOige8lcDFOKwwAdg29U60cIEzHiNHe7x9mD3g4IT47xPPv0-vrj1dv85v2bd1erm9yVFZ_yVleV5NpJJ6EXoi-bRmrVcuXoX7awlEotS1u5TrSidpVVddVKQTP3tixlq86zywPvdm5H6BxJSHYwW1Jj085E683fmeDX5jbeGaUrrZslEbw4EqT4daatmJFWAsNgA8QZjSiFLEtC1gStD1CXImKC_tRGcLM302zMyUyzN9MIachMqnz6p8pT3S_3CPD8CLDo7NAnG5zH3zgpm6asBeFWBxzQTu88JIPOQ3DQ-UTmmy76_xBz-Q-HI0s9tf0CO8BNnBMdBk1ukArMh_3t7U-Pa3rxJVc_ANFM21A</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1512559847</pqid></control><display><type>article</type><title>Effects of aminoguanidine and melatonin on intestinal ischemia/reperfusion injury in rats: An assessor-blinded, controlled experimental study</title><source>DOAJ Directory of Open Access Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>ScienceDirect Journals (5 years ago - present)</source><source>PubMed Central</source><creator>Tunc, Turan, MD ; Kesik, Vural, MD ; Demirin, Hilmi, MD ; Ersoz, Nail, MD ; Vurucu, Sebahattin, MD ; Kul, Mustafa, MD ; Uysal, Bülent, MD ; Sadir, Serdar, MD ; Guven, Ahmet, MD ; Oztas, Emin, MD</creator><creatorcontrib>Tunc, Turan, MD ; Kesik, Vural, MD ; Demirin, Hilmi, MD ; Ersoz, Nail, MD ; Vurucu, Sebahattin, MD ; Kul, Mustafa, MD ; Uysal, Bülent, MD ; Sadir, Serdar, MD ; Guven, Ahmet, MD ; Oztas, Emin, MD</creatorcontrib><description>Abstract Background: The reactive oxygen and nitrogen species generated during reperfusion of tissue are characteristic of intestinal ischemia and reperfusion (IIR) injury. Objective: This study was designed to assess whether the administration of aminoguanidine (AG), a selective nitric oxide synthase inhibitor, and/or melatonin has protective potential in IIR injury. Methods: Male Wistar albino rats (age, 3–4 weeks; weight, 100–150 g) were divided in a nonrandom fashion into 5 groups of equal size: group 1, IIR injury + AG 100 mg/kg; group 2, IIR injury + melatonin 10 mg/kg; group 3, IIR injury + AG 100 mg/kg + melatonin 10 mg/kg; group 4, sham operation; and group 5, IIR injury alone. Sixty minutes of intestinal ischemia and 4 hours of reperfusion were carried out in all but the sham-operation group. Ileal specimens were obtained from all rats to determine the extent of histologic changes, measure tissue concentrations of malondialdehyde (MDA) and protein carbonyl (PC), and assess the activity of superoxide dismutase (SOD) and glutathione peroxidase (GPx). Specimens were also assessed and scored by a pathologist blinded to the experiment and the data. Results: Forty rats were divided into 5 groups of 8 each; all 40 survived until study end. In the IIR injury-alone group, mean (SD) MDA concentration and PC content were significantly higher than that of the sham-operation group, and SOD and GPx activity were significantly lower: MDA concentration, 0.86 (0.03) versus 0.54 (0.01) mmol/g protein, respectively; PC content, 0.60 (0.02) versus 0.34 (0.01) mmol/g protein; SOD activity, 104.33 (43.14) versus 2954.72 (109.55) U/g protein; and GPx activity, 10.44 (0.63) versus 24.34 (1.77) U/g protein (all, P < 0.001). Administration of AG, melatonin, and the AG/melatonin combination was associated with significantly higher SOD (1802.31 [102.35], 1776.50 [58.41], and 1924.28 [98.10] U/g protein, respectively) and GPx (17.36 [1.23], 15.96 [1.08], and 18.06 [1.72] U/g protein) activity and significantly lower MDA concentration (0.62 [0.02], 0.64 [0.02], and 0.56 [0.01] mmol/g protein) and PC content (0.53 [0.03], 0.51 [0.01], and 0.49 [0.02] mmol/g protein) compared with the IIR injury-alone group ( P < 0.001). Mean intestinal mucosal injury scores were significantly lower in the 3 treatment groups (2.12 [0.35], 1.75 [0.46], and 1.12 [0.35]) compared with the IIR injury-alone group (3.87 [0.35]; all, P < 0.001). Conclusion: In this study, AG, melatonin, or both administered in combination were associated with improvements in oxidative markers in this rat model of IIR injury.</description><identifier>ISSN: 0011-393X</identifier><identifier>EISSN: 1879-0313</identifier><identifier>DOI: 10.1016/j.curtheres.2009.12.002</identifier><identifier>PMID: 24692837</identifier><identifier>CODEN: CTCEA9</identifier><language>eng</language><publisher>New York, NY: EM Inc USA</publisher><subject>aminoguanidine ; Biological and medical sciences ; Cardiology. Vascular system ; Gastroenterology. Liver. Pancreas. Abdomen ; Internal Medicine ; intestines ; Medical Education ; Medical sciences ; melatonin ; Other diseases. Semiology ; Pharmacology. Drug treatments ; reperfusion injury ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><ispartof>Current therapeutic research, 2009-12, Vol.70 (6), p.449-459</ispartof><rights>Excerpta Medica Inc.</rights><rights>2009 Excerpta Medica Inc.</rights><rights>2015 INIST-CNRS</rights><rights>2009 The Authors. Published by Elsevier Inc. All rights reserved. 2009 Excerpta Medica Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c560t-b966209c2c2ef11f588293b03c6622be423345a6cd1b17c6a376b21692fa552b3</citedby><cites>FETCH-LOGICAL-c560t-b966209c2c2ef11f588293b03c6622be423345a6cd1b17c6a376b21692fa552b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3969984/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.curtheres.2009.12.002$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,3548,27923,27924,45994,53790,53792</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22288571$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24692837$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tunc, Turan, MD</creatorcontrib><creatorcontrib>Kesik, Vural, MD</creatorcontrib><creatorcontrib>Demirin, Hilmi, MD</creatorcontrib><creatorcontrib>Ersoz, Nail, MD</creatorcontrib><creatorcontrib>Vurucu, Sebahattin, MD</creatorcontrib><creatorcontrib>Kul, Mustafa, MD</creatorcontrib><creatorcontrib>Uysal, Bülent, MD</creatorcontrib><creatorcontrib>Sadir, Serdar, MD</creatorcontrib><creatorcontrib>Guven, Ahmet, MD</creatorcontrib><creatorcontrib>Oztas, Emin, MD</creatorcontrib><title>Effects of aminoguanidine and melatonin on intestinal ischemia/reperfusion injury in rats: An assessor-blinded, controlled experimental study</title><title>Current therapeutic research</title><addtitle>Curr Ther Res Clin Exp</addtitle><description>Abstract Background: The reactive oxygen and nitrogen species generated during reperfusion of tissue are characteristic of intestinal ischemia and reperfusion (IIR) injury. Objective: This study was designed to assess whether the administration of aminoguanidine (AG), a selective nitric oxide synthase inhibitor, and/or melatonin has protective potential in IIR injury. Methods: Male Wistar albino rats (age, 3–4 weeks; weight, 100–150 g) were divided in a nonrandom fashion into 5 groups of equal size: group 1, IIR injury + AG 100 mg/kg; group 2, IIR injury + melatonin 10 mg/kg; group 3, IIR injury + AG 100 mg/kg + melatonin 10 mg/kg; group 4, sham operation; and group 5, IIR injury alone. Sixty minutes of intestinal ischemia and 4 hours of reperfusion were carried out in all but the sham-operation group. Ileal specimens were obtained from all rats to determine the extent of histologic changes, measure tissue concentrations of malondialdehyde (MDA) and protein carbonyl (PC), and assess the activity of superoxide dismutase (SOD) and glutathione peroxidase (GPx). Specimens were also assessed and scored by a pathologist blinded to the experiment and the data. Results: Forty rats were divided into 5 groups of 8 each; all 40 survived until study end. In the IIR injury-alone group, mean (SD) MDA concentration and PC content were significantly higher than that of the sham-operation group, and SOD and GPx activity were significantly lower: MDA concentration, 0.86 (0.03) versus 0.54 (0.01) mmol/g protein, respectively; PC content, 0.60 (0.02) versus 0.34 (0.01) mmol/g protein; SOD activity, 104.33 (43.14) versus 2954.72 (109.55) U/g protein; and GPx activity, 10.44 (0.63) versus 24.34 (1.77) U/g protein (all, P < 0.001). Administration of AG, melatonin, and the AG/melatonin combination was associated with significantly higher SOD (1802.31 [102.35], 1776.50 [58.41], and 1924.28 [98.10] U/g protein, respectively) and GPx (17.36 [1.23], 15.96 [1.08], and 18.06 [1.72] U/g protein) activity and significantly lower MDA concentration (0.62 [0.02], 0.64 [0.02], and 0.56 [0.01] mmol/g protein) and PC content (0.53 [0.03], 0.51 [0.01], and 0.49 [0.02] mmol/g protein) compared with the IIR injury-alone group ( P < 0.001). Mean intestinal mucosal injury scores were significantly lower in the 3 treatment groups (2.12 [0.35], 1.75 [0.46], and 1.12 [0.35]) compared with the IIR injury-alone group (3.87 [0.35]; all, P < 0.001). Conclusion: In this study, AG, melatonin, or both administered in combination were associated with improvements in oxidative markers in this rat model of IIR injury.</description><subject>aminoguanidine</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Internal Medicine</subject><subject>intestines</subject><subject>Medical Education</subject><subject>Medical sciences</subject><subject>melatonin</subject><subject>Other diseases. Semiology</subject><subject>Pharmacology. Drug treatments</subject><subject>reperfusion injury</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><issn>0011-393X</issn><issn>1879-0313</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><recordid>eNqNUsmO1DAQjRCIaQZ-AXxB4kAyXjqLOYzUGg2LNBIHQOJmOU5l2k1iN65kRH8E_0w13TTLiVNZrlevXtWrLHsmeCG4qC42hZvTtIYEWEjOdSFkwbm8ly1EU-ucK6HuZwvOhciVVp_PskeIG855xev6YXYml5WWjaoX2ffrvgc3IYs9s6MP8Xa2wXc-ALOhYyMMdorBBxYD82ECnHywA_Po1jB6e5FgC6mf0f_Mb-a0o8CSnfAVWwVmEQExprwdfOige8lcDFOKwwAdg29U60cIEzHiNHe7x9mD3g4IT47xPPv0-vrj1dv85v2bd1erm9yVFZ_yVleV5NpJJ6EXoi-bRmrVcuXoX7awlEotS1u5TrSidpVVddVKQTP3tixlq86zywPvdm5H6BxJSHYwW1Jj085E683fmeDX5jbeGaUrrZslEbw4EqT4daatmJFWAsNgA8QZjSiFLEtC1gStD1CXImKC_tRGcLM302zMyUyzN9MIachMqnz6p8pT3S_3CPD8CLDo7NAnG5zH3zgpm6asBeFWBxzQTu88JIPOQ3DQ-UTmmy76_xBz-Q-HI0s9tf0CO8BNnBMdBk1ukArMh_3t7U-Pa3rxJVc_ANFM21A</recordid><startdate>20091201</startdate><enddate>20091201</enddate><creator>Tunc, Turan, MD</creator><creator>Kesik, Vural, MD</creator><creator>Demirin, Hilmi, MD</creator><creator>Ersoz, Nail, MD</creator><creator>Vurucu, Sebahattin, MD</creator><creator>Kul, Mustafa, MD</creator><creator>Uysal, Bülent, MD</creator><creator>Sadir, Serdar, MD</creator><creator>Guven, Ahmet, MD</creator><creator>Oztas, Emin, MD</creator><general>EM Inc USA</general><general>Elsevier</general><scope>6I.</scope><scope>AAFTH</scope><scope>IQODW</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20091201</creationdate><title>Effects of aminoguanidine and melatonin on intestinal ischemia/reperfusion injury in rats: An assessor-blinded, controlled experimental study</title><author>Tunc, Turan, MD ; Kesik, Vural, MD ; Demirin, Hilmi, MD ; Ersoz, Nail, MD ; Vurucu, Sebahattin, MD ; Kul, Mustafa, MD ; Uysal, Bülent, MD ; Sadir, Serdar, MD ; Guven, Ahmet, MD ; Oztas, Emin, MD</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c560t-b966209c2c2ef11f588293b03c6622be423345a6cd1b17c6a376b21692fa552b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>aminoguanidine</topic><topic>Biological and medical sciences</topic><topic>Cardiology. Vascular system</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Internal Medicine</topic><topic>intestines</topic><topic>Medical Education</topic><topic>Medical sciences</topic><topic>melatonin</topic><topic>Other diseases. Semiology</topic><topic>Pharmacology. Drug treatments</topic><topic>reperfusion injury</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tunc, Turan, MD</creatorcontrib><creatorcontrib>Kesik, Vural, MD</creatorcontrib><creatorcontrib>Demirin, Hilmi, MD</creatorcontrib><creatorcontrib>Ersoz, Nail, MD</creatorcontrib><creatorcontrib>Vurucu, Sebahattin, MD</creatorcontrib><creatorcontrib>Kul, Mustafa, MD</creatorcontrib><creatorcontrib>Uysal, Bülent, MD</creatorcontrib><creatorcontrib>Sadir, Serdar, MD</creatorcontrib><creatorcontrib>Guven, Ahmet, MD</creatorcontrib><creatorcontrib>Oztas, Emin, MD</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Pascal-Francis</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Current therapeutic research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tunc, Turan, MD</au><au>Kesik, Vural, MD</au><au>Demirin, Hilmi, MD</au><au>Ersoz, Nail, MD</au><au>Vurucu, Sebahattin, MD</au><au>Kul, Mustafa, MD</au><au>Uysal, Bülent, MD</au><au>Sadir, Serdar, MD</au><au>Guven, Ahmet, MD</au><au>Oztas, Emin, MD</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of aminoguanidine and melatonin on intestinal ischemia/reperfusion injury in rats: An assessor-blinded, controlled experimental study</atitle><jtitle>Current therapeutic research</jtitle><addtitle>Curr Ther Res Clin Exp</addtitle><date>2009-12-01</date><risdate>2009</risdate><volume>70</volume><issue>6</issue><spage>449</spage><epage>459</epage><pages>449-459</pages><issn>0011-393X</issn><eissn>1879-0313</eissn><coden>CTCEA9</coden><abstract>Abstract Background: The reactive oxygen and nitrogen species generated during reperfusion of tissue are characteristic of intestinal ischemia and reperfusion (IIR) injury. Objective: This study was designed to assess whether the administration of aminoguanidine (AG), a selective nitric oxide synthase inhibitor, and/or melatonin has protective potential in IIR injury. Methods: Male Wistar albino rats (age, 3–4 weeks; weight, 100–150 g) were divided in a nonrandom fashion into 5 groups of equal size: group 1, IIR injury + AG 100 mg/kg; group 2, IIR injury + melatonin 10 mg/kg; group 3, IIR injury + AG 100 mg/kg + melatonin 10 mg/kg; group 4, sham operation; and group 5, IIR injury alone. Sixty minutes of intestinal ischemia and 4 hours of reperfusion were carried out in all but the sham-operation group. Ileal specimens were obtained from all rats to determine the extent of histologic changes, measure tissue concentrations of malondialdehyde (MDA) and protein carbonyl (PC), and assess the activity of superoxide dismutase (SOD) and glutathione peroxidase (GPx). Specimens were also assessed and scored by a pathologist blinded to the experiment and the data. Results: Forty rats were divided into 5 groups of 8 each; all 40 survived until study end. In the IIR injury-alone group, mean (SD) MDA concentration and PC content were significantly higher than that of the sham-operation group, and SOD and GPx activity were significantly lower: MDA concentration, 0.86 (0.03) versus 0.54 (0.01) mmol/g protein, respectively; PC content, 0.60 (0.02) versus 0.34 (0.01) mmol/g protein; SOD activity, 104.33 (43.14) versus 2954.72 (109.55) U/g protein; and GPx activity, 10.44 (0.63) versus 24.34 (1.77) U/g protein (all, P < 0.001). Administration of AG, melatonin, and the AG/melatonin combination was associated with significantly higher SOD (1802.31 [102.35], 1776.50 [58.41], and 1924.28 [98.10] U/g protein, respectively) and GPx (17.36 [1.23], 15.96 [1.08], and 18.06 [1.72] U/g protein) activity and significantly lower MDA concentration (0.62 [0.02], 0.64 [0.02], and 0.56 [0.01] mmol/g protein) and PC content (0.53 [0.03], 0.51 [0.01], and 0.49 [0.02] mmol/g protein) compared with the IIR injury-alone group ( P < 0.001). Mean intestinal mucosal injury scores were significantly lower in the 3 treatment groups (2.12 [0.35], 1.75 [0.46], and 1.12 [0.35]) compared with the IIR injury-alone group (3.87 [0.35]; all, P < 0.001). Conclusion: In this study, AG, melatonin, or both administered in combination were associated with improvements in oxidative markers in this rat model of IIR injury.</abstract><cop>New York, NY</cop><pub>EM Inc USA</pub><pmid>24692837</pmid><doi>10.1016/j.curtheres.2009.12.002</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | aminoguanidine Biological and medical sciences Cardiology. Vascular system Gastroenterology. Liver. Pancreas. Abdomen Internal Medicine intestines Medical Education Medical sciences melatonin Other diseases. Semiology Pharmacology. Drug treatments reperfusion injury Stomach. Duodenum. Small intestine. Colon. Rectum. Anus |
| title | Effects of aminoguanidine and melatonin on intestinal ischemia/reperfusion injury in rats: An assessor-blinded, controlled experimental study |
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