Mechanistic Effects of Propofol against Renal-ischemia Reperfusion Injury: A Systematic Review

Renal ischemia-reperfusion injury (IRI) is associated with various kidney diseases and dysfunction. This study aims to explore the underlying protective effects of propofol on renal IRI.

This study was conducted on May 20th, 2025, across Web of Science, PubMed/MEDLINE, Scopus, Embase, and the Cochrane Library, to find studies published between 2007 and 2025. Relevant Medical Subject Headings (MeSH) terms and keywords were utilized, and duplicates were removed. A narrative synthesis was performed, and the findings were collected and reviewed.

Propofol significantly reduced renal IRI and decreased serum creatinine, blood urea nitrogen, and histological damage. It enhanced antioxidant defenses and reduced markers of oxidative stress. Propofol also suppressed proinflammatory cytokines and inhibited inflammasome components, including NLRP3, caspase-1, and gasdermin D. Apoptosis was attenuated by lowering the Bcl-2-associated X protein/B-cell lymphoma 2 (Bax/Bcl-2) ratio, caspase-3 activity, and CHOP levels, all involved in apoptosis. Mechanistically, propofol modulated PI3K/AKT/mTOR, MAPK, signal transducer and STAT/PPARγ, and sirtuin 1 signaling pathways.

This review demonstrated that propofol protects against renal IRI by reducing oxidative stress, inflammation, and apoptosis. Beyond its anesthetic role, it may serve as a therapeutic adjunct in contexts, such as transplantation or major surgery. However, further clinical trials are needed to confirm its efficacy, safety, and optimal application in patients.

Propofol demonstrates promising protective effects against renal IRI and may offer benefits in perioperative settings and surgeries with high renal injury risk. However, current evidence remains constrained by methodological limitations in preclinical studies and the scarcity of clinical data.