Proteomics to display tissue repair opposing injury response to LPS-induced liver injury.

摘要: AIM: To examine the protein expression alterations in liver injury/repair network regulation as a response to gut-derived lipopolysaccharide (LPS) treatment, order anticipate possible signal molecules or biomarkers signaling LPS-related injury. METHODS: Male BALB/c mice were treated with intra-peritoneal (i.p.) LPS (4 mg/kg) and sacrificed at 0, 6, 24 30 h obtain livers. The livers stained hematoxylin eosin for histopathologic analyses. Total was separated by two-dimensional gel electrophoresis (2-DE). peptide mass of injury repair related proteins drawn up database searched identify proteins. RESULTS: Observations follows: (1) TRAIL-R2 down regulated LPS-treated mice. TNFAIP1 significantly 6 h, then down-regulated 24, silent during senescent stage. (2) amount metaxin 2 mitochondria import inner membrane translocase subunit TIM8a (TIMM8A) increased upon treatment LPS. (3) P34 cdc2 kinase up-regulated after administration senescent, (4) proteasome activator 28 alpha (PA28), magnesium dependent phosphatase (MDPP) lysophospholipase decreased but recovered treatment. CONCLUSION: mouse displaying time-dependent can result change some proteins.