Genipin Protects Lipopolysaccharide-induced Apoptotic Liver Damage in D-galactosamine-sensitized Mice
- Genipin Protects Lipopolysaccharide-induced Apoptotic Liver Damage in D-galactosamine-sensitized Mice
- 김석주; 김준기; 이동웅; 곽종환; 이선미
- Genipin; Galactosamine/lipopolysaccharide; Apoptosis; Fulminant hepatic failure
- Issue Date
- European journal of pharmacology
- VOL 635, 188-193
- This study examined the effects of genipin, isolated from Gardenia jasminoides Ellis, on D-galactosamine
(GalN) and lipopolysaccharide (LPS)-induced hepatic apoptosis and liver failure. Mice were given an
intraperitoneal injection of genipin (25, 50, 100 and 200 mg/kg) 1 h before GalN (700 mg/kg)/LPS (10 μg/kg)
administration. The survival rate of the genipin group was significantly higher than that of the control.
Genipin markedly reduced the increases in serum aminotransferase activities and lipid peroxidation. The
glutathione content decreased in GalN/LPS group, and this decrease was attenuated by genipin. Increases in
serum tumor necrosis factor-α (TNF-α), which were observed in GalN/LPS-treated mice, were significantly
reduced by genipin. Genipin attenuated the GalN/LPS-induced apoptosis of hepatocytes, as estimated by the
caspase-3 and -8 activity assay, TNF-R1 associated death domain (TRADD) protein measurement and
terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) method. Moreover,
increased cytosolic cytochrome c protein was reduced by genipin. After 3 h of GalN/LPS injection, nuclear
phosphorylated c-Jun (p-c-Jun) level was significantly increased, whereas it was attenuated by genipin. Also,
the increased nuclear level of nuclear factor-κB and the decreased cytosolic level of IκB-α protein were
significantly attenuated by genipin. Our results suggest that genipin offers marked hepatoprotection against
damage induced by GalN/LPS related with its antioxidative, anti-apoptotic activities, and inhibition of NF-κB
nuclear translocation and nuclear p-c-Jun expression.
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