Document Detail


Baicalein inhibits nuclear factor-κB and apoptosis via c-FLIP and MAPK in D-GalN/LPS induced acute liver failure in murine models.
MedLine Citation:
PMID:  20850421     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The hepatoprotective effects and molecular mechanisms of baicalein on acute liver failure induced by d-galactosamine (d-GalN)/lipopolysaccharides (LPS) were investigated in vivo. Mice were administered with different doses of baicalein (50, 100 or 150mg/kg, p.o.) 1h before injection of d-GalN (700mg/kg)/LPS (10μg/kg) and then sacrificed 6h after treatment with d-GalN/LPS. Pretreatment with baicalein prevented d-GalN/LPS-induced liver damage by preventing associated increases of serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) and by reducing serum tumor necrosis factor α (TNF-α), nitric oxide (NO) or inducible nitric oxide synthase (iNOS) expressions. The molecular mechanisms involved in baicalein-induced inhibition of d-GalN/LPS-caused apoptosis were associated with the protection of mitochondria, increasing the Bcl-2/Bax ratio, blocking the release of cytochrome c, and suppressing the phosphorylation of IκBα, ERK and JNK. Moreover, baicalein activated c-FLIP(L), XIAP and cIAP2 proteins, potentially blocking the recruitment of NF-κB signaling molecules. The results support the investigation of baicalein as a therapeutic candidate for acute liver apoptosis or injury and indicate that baicalein might inhibit liver apoptosis by mediating one or more of these pathways.
Authors:
Yan-Ling Wu; Li-Hua Lian; Ying Wan; Ji-Xing Nan
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-09-17
Journal Detail:
Title:  Chemico-biological interactions     Volume:  188     ISSN:  1872-7786     ISO Abbreviation:  Chem. Biol. Interact.     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2010-11-12     Completed Date:  2010-12-21     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0227276     Medline TA:  Chem Biol Interact     Country:  Ireland    
Other Details:
Languages:  eng     Pagination:  526-34     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.
Affiliation:
College of Pharmacy, Yanbian University, Yanji, 133002, Jilin Province, China.
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MeSH Terms
Descriptor/Qualifier:
Alanine Transaminase / blood
Animals
Apoptosis / drug effects*
Aspartate Aminotransferases / blood
CASP8 and FADD-Like Apoptosis Regulating Protein / metabolism*
Caspase 3 / metabolism
Cytochromes c / metabolism
Cytoprotection / drug effects
Disease Models, Animal
Flavanones / pharmacology*
Galactosamine / toxicity
Gene Expression Regulation, Enzymologic / drug effects
Lipopolysaccharides / toxicity
Liver / drug effects,  metabolism,  pathology
Liver Failure / chemically induced*,  metabolism,  pathology*
Male
Mice
Mice, Inbred C57BL
Mitogen-Activated Protein Kinases / metabolism*
NF-kappa B / antagonists & inhibitors*,  metabolism
Nitric Oxide / biosynthesis
Nitric Oxide Synthase Type II / metabolism
Proto-Oncogene Proteins c-bcl-2 / metabolism
Tumor Necrosis Factor-alpha / biosynthesis
X-Linked Inhibitor of Apoptosis Protein / metabolism
Chemical
Reg. No./Substance:
0/CASP8 and FADD-Like Apoptosis Regulating Protein; 0/Cflar protein, mouse; 0/Flavanones; 0/Lipopolysaccharides; 0/NF-kappa B; 0/Proto-Oncogene Proteins c-bcl-2; 0/Tumor Necrosis Factor-alpha; 0/X-Linked Inhibitor of Apoptosis Protein; 10102-43-9/Nitric Oxide; 491-67-8/baicalein; 7535-00-4/Galactosamine; 9007-43-6/Cytochromes c; EC 1.14.13.39/Nitric Oxide Synthase Type II; EC 2.6.1.1/Aspartate Aminotransferases; EC 2.6.1.2/Alanine Transaminase; EC 2.7.11.24/Mitogen-Activated Protein Kinases; EC 3.4.22.-/Caspase 3

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