{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T07:46:47Z","timestamp":1773301607971,"version":"3.50.1"},"reference-count":42,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2000,4,1]],"date-time":"2000-04-01T00:00:00Z","timestamp":954547200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100010578","name":"Deutsche Gesellschaft f\u00fcr Kardiologie-Herz und Kreislaufforschung.","doi-asserted-by":"publisher","award":["FS\/96018"],"award-info":[{"award-number":["FS\/96018"]}],"id":[{"id":"10.13039\/501100010578","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["faseb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FASEB Journal"],"published-print":{"date-parts":[[2000,4]]},"abstract":"<jats:p>\n                    The activation of poly (ADP\u2010ribose) synthetase (PARS) subsequent to DNA damage caused by reactive oxygen or nitrogen species has been implicated in several pathophysiological conditions, including ischemia\u2010reperfusion injury and shock. The aim of this study was to investigate whether PARS inhibitors could provide protection against renal ischemia\u2010reperfusion injury in the rat\n                    <jats:italic>in vivo.<\/jats:italic>\n                    Male Wistar rats were subjected to 45 min bilateral clamping of the renal pedicles, followed by 6 h reperfusion (control animals). Animals were administered the PARS inhibitors 3\u2010aminobenz\u2010amide, 1,5\u2010dihydroxyisoquinoline, or nicotinamide during the reperfusion period. Ischemia, followed by reperfusion, produced significant increases in plasma concentrations of urea, creatinine, and fractional excretion of Na\n                    <jats:sup>+<\/jats:sup>\n                    (FE\n                    <jats:sub>Na<\/jats:sub>\n                    ) and produced a significant reduction in glomerular filtration rate (GFR). However, administration of the PARS inhibitors significantly reduced urea and creatinine concentrations, suggesting improved renal function. The PARS inhibitors also significantly increased GFR and reduced FE\n                    <jats:sub>Na<\/jats:sub>\n                    , suggesting the recovery of both glomerular and tubular function, respectively, with a more pronounced recovery of tubular function. In kidneys from control animals, histological examination revealed severe renal damage and immunohistochemical localization demonstrated PARS activation in the proximal tubule. Both renal damage and PARS activation were attenuated by administration of PARS inhibitors during reperfusion. Therefore, we propose that PARS activation contributes to renal reperfusion injury and that PARS inhibitors may be beneficial in renal disorders associated with oxidative stress\u2010mediated injury.\u2014Chatterjee, P. K., Zacha\u2010rowski, K., Cuzzocrea, S., Otto, M., Thiemermann, C. Inhibitors of poly (ADP\u2010ribose) synthetase reduce renal ischemia\u2010reperfusion injury in the anesthetized rat\n                    <jats:italic>in vivo. FASEB J.<\/jats:italic>\n                    14, 641\u2013651 (2000)\n                  <\/jats:p>","DOI":"10.1096\/fasebj.14.5.641","type":"journal-article","created":{"date-parts":[[2018,1,18]],"date-time":"2018-01-18T08:32:05Z","timestamp":1516264325000},"page":"641-651","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":90,"title":["Inhibitors of poly (ADP\u2010ribose) synthetase reduce renal ischemia\u2010reperfusion injury in the anesthetized rat\n                    <i>in vivo<\/i>"],"prefix":"10.1096","volume":"14","author":[{"given":"Prabal K.","family":"Chatterjee","sequence":"first","affiliation":[{"name":"The William Harvey Research Institute St. Bartholomew's and the Royal London School of Medicine and Dentistry  London EC1M 6BQ U.K."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kai","family":"Zacharowski","sequence":"additional","affiliation":[{"name":"The William Harvey Research Institute St. Bartholomew's and the Royal London School of Medicine and Dentistry  London EC1M 6BQ U.K."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Salvatore","family":"Cuzzocrea","sequence":"additional","affiliation":[{"name":"Institute of Pharmacology University of Messina  Messina 98123 Italy"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mike","family":"Otto","sequence":"additional","affiliation":[{"name":"Institute of Pathology University of Mainz  Mainz D\u201055101 Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Christoph","family":"Thiemermann","sequence":"additional","affiliation":[{"name":"The William Harvey Research Institute St. Bartholomew's and the Royal London School of Medicine and Dentistry  London EC1M 6BQ U.K."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2000,4]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199605303342207"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.3.F477"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2168.1996.02182.x"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.80.5.1115"},{"key":"e_1_2_6_6_1","first-page":"632","article-title":"The cell biology of reperfusion injury in the kidney","volume":"42","author":"Paller M. 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