title: Hypothermia is better than ischemic preconditioning for preventing early hepatic ischemia/reperfusion in rats.
abstract: BACKGROUND
  Topical hypothermia (TH) and ischemic preconditioning (IPC) are used to decrease I/R injury. The efficacy of isolated or combined use of TH and IPC in the liver regarding inflammation and cytoprotection in early ischemia/reperfusion (I/R) injury needs to be evaluated.
  
  
  METHODS
  Wistar rats underwent 70% liver ischemia for 90 min followed by 120 min of reperfusion. Livers of animals allocated in the sham, normothermic ischemia (NI), IPC, TH, and TH+IPC groups were collected for molecular analyses by ELISA and Western blot, aiming to compare proinflammatory, anti-inflammatory, and antioxidant profiles.
  
  
  RESULTS
  Compared with NI, TH presented decreased tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6 and IL-12 concentrations and increased IL-10 levels. TH animals displayed lower inducible nitric oxide synthase (iNOS) and higher endothelial nitric oxide synthase (eNOS) expressions. NAD(P)H-quinone oxidoreductase-1(NQO1) expression was also lower with TH. Isolated IPC and NI were similar regarding all these markers. TH+IPC was associated with decreased IL-12 concentration and reduced iNOS and NQO1 expressions, similarly to isolated TH. Expression of Kelch-like ECH-associated protein (Keap)-1 was increased and expression of nuclear and cytosolic nuclear erythroid 2-related factor 2 (Nrf2) was decreased with TH+IPC vs. NI.
  
  
  CONCLUSIONS
  TH was the most effective method of protection against early I/R injury. Isolated IPC entailed triggering of second-line antioxidant defense enzymes. Combined TH+IPC seemed to confer no additional advantage over isolated TH in relation to the inflammatory process, but had the advantage of completely avoid second-line antioxidant defense enzymes.
authors.affiliation: Graduate Program in Gastroenterology and Hepatology, Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre, Brazil.
authors.forename: Larisse
authors.initials: L
authors.lastname: Longo
authors.affiliation: Graduate Program in Gastroenterology and Hepatology, Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre, Brazil.
authors.forename: Leila Xavier
authors.initials: LX
authors.lastname: Sinigaglia-Fratta
authors.affiliation: Graduate Program in Gastroenterology and Hepatology, Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre, Brazil.
authors.forename: Giovana R
authors.initials: GR
authors.lastname: Weber
authors.affiliation: Experimental Laboratory of Hepatology and Gastroenterology,Porto Alegre, Brazil.
authors.forename: Andrea
authors.initials: A
authors.lastname: Janz-Moreira
authors.affiliation: Gene Therapy Center,Porto Alegre, Brazil.
authors.forename: Nélson A
authors.initials: NA
authors.lastname: Kretzmann
authors.affiliation: Surgery Unit, Porto Alegre, Brazil.
authors.forename: Tomaz de J M
authors.initials: Tde J
authors.lastname: Grezzana-Filho
authors.affiliation: Experimental Laboratory of Hepatology and Gastroenterology,Porto Alegre, Brazil.
authors.forename: Norma
authors.initials: N
authors.lastname: Possa-Marroni
authors.affiliation: Surgery Unit, Porto Alegre, Brazil.
authors.forename: Carlos O
authors.initials: CO
authors.lastname: Corso
authors.affiliation: Pathology Unit, Porto Alegre, Brazil.
authors.forename: Carlos T
authors.initials: CT
authors.lastname: Schmidt-Cerski
authors.affiliation: Experimental Laboratory of Hepatology and Gastroenterology,Porto Alegre, Brazil.
authors.forename: Themis
authors.initials: T
authors.lastname: Reverbel-da-Silveira
authors.affiliation: Graduate Program in Gastroenterology and Hepatology, Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre, Brazil.
authors.forename: Mário R
authors.initials: MR
authors.lastname: Álvares-da-Silva
authors.affiliation: Experimental Laboratory of Hepatology and Gastroenterology,Porto Alegre, Brazil.
authors.forename: Jorge L
authors.initials: JL
authors.lastname: dos-Santos
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D007036:Hypothermia, Induced; D018836:Inflammation Mediators / Q000378:metabolism; D047908:Intracellular Signaling Peptides and Proteins / Q000378:metabolism; D019194:Ischemic Preconditioning; D000072019:Kelch-Like ECH-Associated Protein 1; D008099:Liver / Q000098:blood supply* / Q000378:metabolism / Q000473:pathology; D008297:Male; D016660:NAD(P)H Dehydrogenase (Quinone) / Q000378:metabolism; D051267:NF-E2-Related Factor 2 / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*
chemical_list: D000975:Antioxidants; D016207:Cytokines; D018836:Inflammation Mediators; D047908:Intracellular Signaling Peptides and Proteins; C486610:KEAP1 protein, rat; D000072019:Kelch-Like ECH-Associated Protein 1; D051267:NF-E2-Related Factor 2; C495637:Nfe2l2 protein, rat; D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III; C496318:Nos2 protein, rat; C496316:Nos3 protein, rat; D016660:NAD(P)H Dehydrogenase (Quinone); C507703:NQO1 protein, rat