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- Title
Immune neutralization of the receptor for advanced glycation end products reduce liver oxidative damage induced by an acute systemic injection of lipopolysaccharide.
- Authors
Tiefensee Ribeiro, Camila; Gasparotto, Juciano; Alves Teixeira, Alexsander; Cruz Portela, Luis Valmor; Louzada Flores, Viviane Noll; Fonseca Moreira, José Claudio; Pens Gelain, Daniel
- Abstract
The receptor for advanced glycation end products (RAGE) is a multi-ligand receptor, which activation amplifies and perpetuates inflammatory reactions. RAGE activation also strongly stimulates the production of reactive oxygen species, leading an imbalance of redox cellular state. The extent of liver damage caused by inflammation is crucial to the systemic response during proinflammatory episodes. To investigate the role of RAGE in liver damage caused by systemic inflammation, we evaluated the effect of RAGE blocking in oxidative stress parameters induced by systemic lipopolysaccharide (LPS) injection. Wistar rats received an intraperitoneal injection of RAGE antibody (50 mg/kg), 1 h prior intraperitoneal injection of LPS (5 mg/kg). Twenty-four hours later, the liver was isolated for analysis. The LPS-induced effect in protein oxidative damage, mitochondrial complex II activity, catalase activity, signal transducer and activator of transcription 3 phosphorylation and caspase 3 activation was prevented by prior treatment with RAGE antibody. However, RAGE blocking was not able to inhibit reactive oxygen species production and the impairment in nonenzymatic antioxidant capacity induced by LPS. The present results indicate that RAGE is an important mediator of liver oxidative damage induced by an acute systemic injection of LPS, although other mechanisms may also be responsible for liver function impairment during inflammation.
- Subjects
ADVANCED glycation end-products; OXIDATIVE stress; LIPOPOLYSACCHARIDES; REACTIVE oxygen species; SYSTEMIC inflammatory response syndrome; LABORATORY rats
- Publication
Journal of Biochemistry, 2018, Vol 163, Issue 6, p515
- ISSN
0021-924X
- Publication type
Article
- DOI
10.1093/jb/mvy013