Protection against in vivo liver ischemia-reperfusion injury by n-3 long-chain polyunsaturated fatty acids in the rat

• Published in: Free radical research 2010-08, Vol.44 (8), p.854-863
• Main Authors: Zúñiga, Jessica, Venegas, Francisca, Villarreal, Marcela, Núñez, Daniel, Chandía, Marlene, Valenzuela, Rodrigo, Tapia, Gladys, Varela, Patricia, Videla, Luis A., Fernández, Virginia
• Format: Article
• Language: English
• Subjects: Animals; Cytokines - blood; Cytokines - immunology; Dietary Supplements; DNA - drug effects; Fatty Acids, Omega-3 - administration & dosage; Fatty Acids, Omega-3 - pharmacology; Ischemia-reperfusion injury; Liver - drug effects; Liver - immunology; Liver - pathology; liver preconditioning; Male; n-3 polyunsaturated fatty acid; NF-kappa B - genetics; NF-kappa B - immunology; NF-κB activation; oxidative stress; Oxidative Stress - drug effects; pro-inflammatory cytokines; Rats; Rats, Sprague-Dawley; Reperfusion Injury - immunology; Reperfusion Injury - prevention & control
• ISSN: 1071-5762; 1029-2470
• DOI: 10.3109/10715762.2010.485995

Abstract N-3 polyunsaturated fatty acids (n-3 PUFA) affect inflammatory processes. This study evaluated the effects of dietary supplementation with fish oil on hepatic ischemia-reperfusion (IR) injury in the rat. Parameters of liver injury (serum transaminases and histology) and oxidative stress (serum 8-isoprostanes and hepatic GSH and GSSG), were correlated with NF-κB DNA binding and FA composition and inflammatory cytokine release. N-3 PUFA supplementation significantly increased liver n-3 PUFA content and decreased n-6/n-3 PUFA ratios. IR significantly modified liver histology and enhanced serum transaminases, 8-isoprotanes and inflammatory cytokines, with net reduction in liver GSH levels and net increment in those of GSSG. Early increase (3 h) and late reduction (20 h) in NF-κB activity was induced. All IR-induced changes were normalized by n-3 PUFA supplementation. In conclusion, prevention of liver IR-injury was achieved by n-3 PUFA supplementation, with suppression of oxidative stress and recovery of pro-inflammatory cytokine homeostasis and NF-κB functionality lost during IR.