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Updated: Nov 2, 2025
Renal Ischaemia Reperfusion Injury: A Mouse Model of Injury and Regeneration
Published on: June 7, 2014
Propofol ameliorates renal ischemia/reperfusion injury by enhancing macrophage M2 polarization through PPARγ/STAT3
Zhaohui Liu1, Yanli Meng2, Yu Miao3
1Department of Anesthesiology, Cangzhou Central Hospital, Cangzhou, Hebei, China.
Abstract:
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.
Insights
Propofol protects kidneys from ischemia/reperfusion injury by promoting anti-inflammatory M2 macrophage polarization via the PPARγ/STAT3 pathway. This study reveals a novel mechanism for propofol
Area of Science:
- Nephrology
- Immunology
- Pharmacology
Background:
- Renal ischemia/reperfusion (rI/R) injury is a significant clinical challenge.
- Propofol (Pro) offers renoprotection through incompletely understood mechanisms.
- Propofol exhibits anti-inflammatory properties, suggesting a role in modulating immune responses.
Purpose of the Study:
- To investigate propofol's effect on macrophage polarization during rI/R injury.
- To elucidate the molecular pathways involved in propofol-mediated renoprotection.
Main Methods:
- Rats underwent rI/R surgery with propofol or vehicle administration.
- Cultured peritoneal macrophages (PMs) were exposed to hypoxia/reoxygenation (H/R).
- Macrophage polarization markers, STAT signaling, and PPARγ were analyzed using molecular techniques.
Main Results:
- Propofol attenuated kidney damage and reduced pro-inflammatory cytokines (TNF-α, IL-6, CXCL-10) post-rI/R.
- Propofol enhanced M2 macrophage polarization (increased Arg1, Mrc1; decreased iNOS) in vivo and in vitro.
- Propofol upregulated p-STAT3, p-STAT6, and PPARγ, while downregulating p-STAT1 in H/R-treated PMs.
- PPARγ silencing abolished propofol-induced STAT3 activation and M2 polarization.
Conclusions:
- Propofol confers renoprotection against rI/R injury.
- Propofol promotes M2 macrophage polarization through a PPARγ/STAT3-dependent mechanism.
- Targeting macrophage polarization represents a potential therapeutic strategy for rI/R injury.
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