title: Protective effects of propofol on endotoxemia-induced acute kidney injury in rats.
abstract: 1. Animal studies suggest that propofol protects against endotoxaemia-induced lung and kidney injury. Upregulation of aquaporin expression in lung tissue mediates these effects, but the mechanism of action in the kidney is unclear. The present study examined the protective effects of propofol on endotoxaemia-induced acute kidney injury in rats. 2. A rat model of endotoxaemia was established using lipopolysaccharide (LPS). We determined the effects of 10% propofol administration 1 h before, during and 1 h after LPS-induced endotoxaemia on expression of aquaporin (AQP)-2, tumour necrosis factor (TNF)-α, intercellular adhesion molecule (ICAM)-1, caspase 3, Bcl-2 and Bax using reverse transcription-polymerase chain reaction, western blotting and immunocytochemistry. Renal morphology, superstructure, apoptosis and function were also assessed. 3. Normal renal tubular structure was seen in the propofol pretreated group, but LPS treatment resulted in changes to renal tissue morphology. Propofol treatment improved renal function in LPS-treated rats. Pretreatment with propofol 1 h before LPS normalized urine and serum osmolality, serum creatinine and blood urea nitrogen to control levels. Lipopolysaccharide downregulated expression of AQP-2 and downregulated the expression of ICAM-1 and TNF-α. These effects were reversed by propofol treatment. Lipopolysaccharide reduced the Bcl2 : Bax ratio and induced renal cell apoptosis and these effects were reduced by propofol treatment. Overall, propofol pretreatment had greater effects than concurrent treatment or propofol administration after LPS induction of endotoxaemia. 4. In conclusion, propofol pretreatment protected renal function in a rat model of endotoxaemia. Further studies are necessary to confirm this effect in other experimental models and in humans.
authors.affiliation: Department of Anaesthesiology, The First University Hospital of China Medical University, Shenyang, China.
authors.forename: Wen-Yao
authors.initials: WY
authors.lastname: Cui
authors.forename: A-Yong
authors.initials: AY
authors.lastname: Tian
authors.forename: Tao
authors.initials: T
authors.lastname: Bai
mesh_terms: D058186:Acute Kidney Injury / Q000139:chemically induced / Q000188:drug therapy* / Q000235:genetics / Q000473:pathology; D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000235:genetics; D020346:Aquaporins / Q000096:biosynthesis / Q000235:genetics; D001806:Blood Urea Nitrogen; D053148:Caspase 3 / Q000096:biosynthesis / Q000235:genetics; D003404:Creatinine / Q000097:blood; D015536:Down-Regulation / Q000235:genetics; D019446:Endotoxemia / Q000139:chemically induced / Q000188:drug therapy* / Q000235:genetics / Q000473:pathology; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis / Q000235:genetics; D007684:Kidney Tubules / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D008070:Lipopolysaccharides; D008297:Male; D015742:Propofol / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism; D015854:Up-Regulation; D051028:bcl-2-Associated X Protein / Q000096:biosynthesis / Q000235:genetics
chemical_list: D020346:Aquaporins; C494828:Bax protein, rat; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D051028:bcl-2-Associated X Protein; D018799:Intercellular Adhesion Molecule-1; D003404:Creatinine; C505410:Casp3 protein, rat; D053148:Caspase 3; D015742:Propofol