ReferenceID 500
Afzelin ameliorates D-galactosamine and lipopolysaccharide-induced fulminant hepatic failure by modulating mitochondrial quality control and dynamics
Br J Pharmacol
BACKGROUND AND PURPOSE: Fulminant hepatic failure (FHF) is a fatal clinical syndrome that results in excessive inflammation and hepatocyte death. Mitochondrial dysfunction is considered to be a possible mechanism of FHF.
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Record Fields
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- Reference Id
- 500
- Evidence Id
- 17090
- Core Evidence Id
- 17090
- Source Reference Id
- 976
- Herb2 Reference Id
- HBREF001687
- Subject Paper Key
- HBIN014792_27861739
- Pubmed Id
- 27861739
- Doi
- 10.1111/bph.13669
- Paper Title
- Afzelin ameliorates D-galactosamine and lipopolysaccharide-induced fulminant hepatic failure by modulating mitochondrial quality control and dynamics
- Paper Abstract
- BACKGROUND AND PURPOSE: Fulminant hepatic failure (FHF) is a fatal clinical syndrome that results in excessive inflammation and hepatocyte death. Mitochondrial dysfunction is considered to be a possible mechanism of FHF. Afzelin, a flavonol glycoside found in Houttuynia cordata Thunberg, has anti-inflammatory and antioxidant properties. The present study elucidated the cytoprotective mechanisms of afzelin against D-galactosamine (GalN)/LPS induced FHF, particularly focusing on mitochondrial quality control and dynamics. EXPERIMENTAL APPROACH: Mice were administered afzelin i.p. 1 h before receiving GalN (800 mg·kg-1 )/LPS (40 μg·kg-1 ), and they were then killed 5 h after GalN/LPS treatment. KEY RESULTS: Afzelin improved the survival rate and reduced the serum levels of alanine aminotransferase and pro-inflammatory cytokines in GalN/LPS-treated mice. Afzelin attenuated the mitochondrial damage, as indicated by diminished mitochondrial swelling and mitochondrial glutamate dehydrogenase activity in GalN/LPS-treated mice. Afzelin enhanced mitochondrial biogenesis, as indicated by increased levels of PPAR-γ coactivator 1α, nuclear respiratory factor 1 and mitochondrial transcription factor A. Afzelin also decreased the level of mitophagy-related proteins, parkin and PTEN-induced putative kinase 1. Furthermore, while GalN/LPS significantly increased the level of fission-related protein, dynamin-related protein 1, and decreased the level of fusion-related protein, mitofusin 2; these effects were attenuated by afzelin. CONCLUSIONS AND IMPLICATIONS: Our findings demonstrated that afzelin protects against GalN/LPS-induced liver injury by enhancing mitochondrial biogenesis, suppressing excessive mitophagy and balancing mitochondrial dynamics.
- Journal
- Br J Pharmacol
- Publish Year
- 2017
- Experiment Subject
- mouse
- Experiment Type
- Animal Experiment
- Phenotype Related
- Paper Title Cn
- Paper Title En
- Afzelin ameliorates D-galactosamine and lipopolysaccharide-induced fulminant hepatic failure by modulating mitochondrial quality control and dynamics
- Bilingual Status
- semi_complete