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This study was to investigate the protective effect of intestinal ischemic postconditioning (IPo) on IIR\u2010induced acute kidney injury (AKI) and the underling cellular signaling mechanisms with focus on the Nrf2\/HO\u20101. Adult C57BL\/6J mice were subjected to IIR with or without IPo. IIR was established by clamping the superior mesenteric artery (SMA) for 45\u00a0minutes followed by 120\u00a0minutes reperfusion. Outcome measures were: (i) Intestinal and renal histopathology; (ii) Renal function; (iii) Cellular signaling changes; (iv) Oxidative stress and inflammatory responses. IPo significantly attenuated IIR\u2010induced kidney injury. Furthermore, IPo significantly increased both nuclear Nrf2 and HO\u20101 expression in the kidney, upregulated autophagic flux, inhibited IIR\u2010induced inflammation and reduced oxidative stress. The protective effect of IPo was abolished by the administration of Nrf2 inhibitor (Brusatol) or Nrf2 siRNA. Conversely, a Nrf2 activator t\u2010BHQ has a similar protective effect to that of IPo. Our data indicate that IPo protects the kidney injury induced by IIR, which was likely mediated through the Nrf2\/HO\u20101 cellular signaling activation.<\/jats:p>","DOI":"10.1096\/fj.202000274r","type":"journal-article","created":{"date-parts":[[2020,7,27]],"date-time":"2020-07-27T10:37:08Z","timestamp":1595846228000},"page":"8887-8901","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":25,"title":["RETRACTED: Ischemic postconditioning attenuates acute kidney injury following intestinal ischemia\u2010reperfusion through Nrf2\u2010regulated autophagy, anti\u2010oxidation, and anti\u2010inflammation in mice"],"prefix":"10.1096","volume":"34","author":[{"given":"Rong","family":"Chen","sequence":"first","affiliation":[{"name":"Department of Anesthesiology Renmin Hospital of Wuhan University Wuhan 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