Research Paper Volume 13, Issue 11 pp 15511—15522

Propofol ameliorates renal ischemia/reperfusion injury by enhancing macrophage M2 polarization through PPARγ/STAT3 signaling

Zhaohui Liu1, , Yanli Meng2, , Yu Miao3, , Lili Yu1, , Qianjie Wei1, , Yuqing Li4, , Bing Zhang4, , Qiannan Yu1, ,

  • 1 Department of Anesthesiology, Cangzhou Central Hospital, Cangzhou, Hebei, China
  • 2 Department of Gastroenterology, Cangzhou Central Hospital, Cangzhou, Hebei, China
  • 3 Department of Neurosurgery, Cangzhou Central Hospital, Cangzhou, Hebei, China
  • 4 Department of Anesthesiology, Botou Hospital, Botou, Cangzhou, Hebei, China

Received: December 18, 2020       Accepted: May 13, 2021       Published: June 10, 2021
How to Cite

Copyright: © 2021 Liu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


Propofol (Pro) confers protection against renal ischemia/reperfusion (rI/R) injury through incompletely characterized mechanisms. Since Pro has shown net anti-inflammatory properties as part of its beneficial effects, we examined the potential role of Pro in the modulation of macrophage polarization status during both rI/R injury in vivo and exposure of cultured peritoneal macrophages (PMs) to hypoxia/reoxygenation (H/R). Rats were subjected to 45-min r/IR surgery or a sham procedure and administered PBS (vehicle) or Pro during the ischemia stage. Pro administration attenuated rI/R-induced kidney damage and renal TNF-α, IL-6, and CXCL-10 expression. Enhanced macrophage M2 polarization, evidenced by reduced iNOS and increased Arg1 and Mrc1 mRNA levels, was further detected after Pro treatment both in the kidney, after rI/R in vivo, and in H/R-treated PMs. Pro administration also repressed phosphorylated signal transducer and activator of transcription 1 (p-STAT1) and increased p-STAT3, p-STAT6, and peroxisome proliferator-activated receptor-γ (PPARγ) mRNA levels in H/R-exposed PMs. Importantly, siRNA-mediated PPARγ silencing repressed Pro-mediated STAT3 activation in PMs and restored proinflammatory cytokine levels and prevented macrophage M2 marker expression in both rI/R-treated rats and cultured PMs. These findings suggest that Pro confers renoprotection against rI/R by stimulating PPARγ/STAT3-dependent macrophage conversion to the M2 phenotype.


Pro: propofol; rI/R: renal ischemia/reperfusion; PMs: peritoneal macrophages; H/R: hypoxia/reoxygenation.