{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T00:22:27Z","timestamp":1791073347726,"version":"4.1.0"},"reference-count":47,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2009,2,17]],"date-time":"2009-02-17T00:00:00Z","timestamp":1234828800000},"content-version":"vor","delay-in-days":1630,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2004,9]]},"abstract":"<jats:p>\n<jats:list list-type=\"explicit-label\">\n<jats:list-item><jats:p>Neutrophils are thought to play a major role in the mediation of reperfusion injury. CXC chemokines are known inducers of neutrophil recruitment. Here, we assessed the effects of Repertaxin, a novel low molecular weight inhibitor of human CXCL8 receptor activation, on the local, remote and systemic injuries following intestinal ischaemia and reperfusion (I\/R) in the rat.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Pre\u2010incubation of rat neutrophils with Repertaxin (10<jats:sup>\u221211<\/jats:sup>\u201310<jats:sup>\u22126<\/jats:sup><jats:sc>M<\/jats:sc>) inhibited the chemotaxis of neutrophils induced by human CXCL8 or rat CINC\u20101, but not that induced by fMLP, PAF or LTB<jats:sub>4<\/jats:sub>, in a concentration\u2010dependent manner. Repertaxin also prevented CXCL8\u2010induced calcium influx but not CXCL8 binding to purified rat neutrophils.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>In a model of mild I\/R injury (30 min of ischaemia and 30 min of reperfusion), Repertaxin dose\u2010dependently (3\u201330 mg kg<jats:sup>\u22121<\/jats:sup>) inhibited the increase in vascular permeability and neutrophil influx. Maximal inhibition occurred at 30 mg kg<jats:sup>\u22121<\/jats:sup>.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Following severe I\/R injury (120 min of ischaemia and 120 min of reperfusion), Repertaxin (30 mg kg<jats:sup>\u22121<\/jats:sup>) markedly prevented neutrophil influx, the increase in vascular permeability both in the intestine and the lungs. Moreover, there was prevention of haemorrhage in the intestine of reperfused animals.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Repertaxin effectively suppressed the increase in tissue (intestine and lungs) and serum concentrations of TNF\u2010<jats:italic>\u03b1<\/jats:italic> and the reperfusion\u2010associated lethality.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>For comparison, we also evaluated the effects of an anti\u2010CINC\u20101 antibody in the model of severe I\/R injury. Overall, the antibody effectively prevented tissue injury, systemic inflammation and lethality. However, the effects of the antibody were in general of lower magnitude than those of Repertaxin.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>In conclusion, CINC\u20101 and possibly other CXC chemokines, acting on CXCR2, have an important role during I\/R injury. Thus, drugs, such as Repertaxin, developed to block the function of the CXCR2 receptor may be effective at preventing reperfusion injury in relevant clinical situations.<\/jats:p><\/jats:list-item>\n<\/jats:list>\n<\/jats:p><jats:p> <jats:italic>British Journal of Pharmacology<\/jats:italic> (2004) <jats:bold>143<\/jats:bold>, 132\u2013142. doi:<jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" xlink:href=\"10.1038\/sj.bjp.0705862\">10.1038\/sj.bjp.0705862<\/jats:ext-link><\/jats:p>","DOI":"10.1038\/sj.bjp.0705862","type":"journal-article","created":{"date-parts":[[2004,9,2]],"date-time":"2004-09-02T20:31:48Z","timestamp":1094157108000},"page":"132-142","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":100,"title":["Repertaxin, a novel inhibitor of rat CXCR2 function, inhibits inflammatory responses that follow intestinal ischaemia and reperfusion injury"],"prefix":"10.1111","volume":"143","author":[{"given":"Danielle G","family":"Souza","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Riccardo","family":"Bertini","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Angelica T","family":"Vieira","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fernando Q","family":"Cunha","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steve","family":"Poole","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marcello","family":"Allegretti","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Francesco","family":"Colotta","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mauro M","family":"Teixeira","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2009,2,17]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/0192-0561(94)00088-6"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1007\/s00395-002-0366-7"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0402090101"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.1016\/0022-1759(87)90363-2"},{"key":"e_1_2_7_6_1","doi-asserted-by":"crossref","first-page":"2388","DOI":"10.1182\/blood.V86.6.2388.bloodjournal8662388","article-title":"Single\u2010cell analysis of macrophage chemotactic protein\u20101\u2010regulated cytosolic Ca2+ increase in human adherent monocytes","volume":"86","author":"BIZZARRI C.","year":"1995","journal-title":"Blood"},{"key":"e_1_2_7_7_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-2952(01)00610-4"},{"key":"e_1_2_7_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5223(98)70249-1"},{"key":"e_1_2_7_9_1","doi-asserted-by":"publisher","DOI":"10.1002\/jlb.59.3.427"},{"key":"e_1_2_7_10_1","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.103.18.2296"},{"key":"e_1_2_7_11_1","doi-asserted-by":"publisher","DOI":"10.1016\/S1054-3589(08)60070-8"},{"key":"e_1_2_7_12_1","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.148.7.2133"},{"key":"e_1_2_7_13_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0014-2999(00)00330-7"},{"key":"e_1_2_7_14_1","doi-asserted-by":"publisher","DOI":"10.1006\/jsre.1996.0101"},{"key":"e_1_2_7_15_1","doi-asserted-by":"publisher","DOI":"10.1677\/jme.0.0110031"},{"key":"e_1_2_7_16_1","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.4.15.2253850"},{"key":"e_1_2_7_17_1","first-page":"II401","article-title":"Induction of interleukin\u20108 expression during cardiopulmonary bypass","volume":"88","author":"KALFIN R.E.","year":"1993","journal-title":"Circulation"},{"key":"e_1_2_7_18_1","doi-asserted-by":"publisher","DOI":"10.1097\/00007890-200206150-00007"},{"key":"e_1_2_7_19_1","doi-asserted-by":"publisher","DOI":"10.1159\/000063073"},{"key":"e_1_2_7_20_1","doi-asserted-by":"publisher","DOI":"10.1152\/jappl.1999.87.6.2357"},{"key":"e_1_2_7_21_1","first-page":"H88","article-title":"Effects of a monoclonal antibody directed against P\u2010selectin after myocardial ischemia and reperfusion","volume":"270","author":"LEFER D.J.","year":"1996","journal-title":"Am. 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