Ischemic postconditioning attenuates acute kidney injury following intestinal ischemia-reperfusion through Nrf2-regulated autophagy, anti-oxidation, and anti-inflammation in mice.
MouseIschaemia-reperfusionRenalC57BL/6JMaleNot applicable, surgical conditioningAt the onset of reperfusion
Model: Intestinal ischaemia-reperfusion by clamping the superior mesenteric artery for 45 minutes followed by 120 minutes reperfusion, causing acute kidney injury
Ischaemic postconditioning attenuated kidney injury after intestinal ischaemia-reperfusion, increased nuclear Nrf2 and HO-1, upregulated autophagic flux and reduced inflammation and oxidative stress; the protection was abolished by brusatol or Nrf2 siRNA and reproduced by t-BHQ.
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