10.1021/np2003935.s001
Woo-Cheol Lee
Woo-Cheol
Lee
Hyun Ah Jung
Hyun Ah
Jung
Jae Sue Choi
Jae Sue
Choi
Yeong Shik Kim
Yeong Shik
Kim
Sun-Mee Lee
Sun-Mee
Lee
Protective Effects of Luteolin against Apoptotic Liver Damage Induced by d-Galactosamine/Lipopolysaccharide in Mice
American Chemical Society
2011
serum level
cytochrome c protein expression
BH
LPS
Cirsium japonicum
intraperitoneal injection
GalN
apoptotic pathways
Apoptotic Liver Damage Induced
Protective Effects
TNF
1 attenuated apoptosis
1. Treatment
protein expression
serum aminotransferase activity
2011-09-23 00:00:00
Journal contribution
https://acs.figshare.com/articles/journal_contribution/Protective_Effects_of_Luteolin_against_Apoptotic_Liver_Damage_Induced_by_d_Galactosamine_Lipopolysaccharide_in_Mice/2611684
In this study, the protective effects of luteolin (<b>1</b>, a major component of <i>Cirsium japonicum</i>) were examined against d-galactosamine (GalN)/lipopolysaccharide (LPS)-induced fulminant hepatic failure. Mice received an intraperitoneal injection of <b>1</b> (25, 50, 100, and 200 mg<b>·</b>kg<sup>–1</sup>) 1 h before treatment with GalN (700 mg<b>·</b>kg<sup>–1</sup>)/LPS (10 μg<b>·</b>kg<sup>–1</sup>). Treatment with GalN/LPS resulted in increased mortality and serum aminotransferase activity. These increases were attenuated by pretreatment with <b>1</b>. Treatment with GalN/LPS induced an increase in the serum level of tumor necrosis factor-α (TNF-α) and protein expression of TNF-α receptor-associated death domain, and these increases were prevented by <b>1</b>. In addition, <b>1</b> attenuated apoptosis induced by GalN/LPS treatment, which was analyzed using a caspase-3 and -8 activity assay, as well as by proapoptotic BH3-only protein and cytochrome <i>c</i> protein expression, and by a terminal deoxynuleotidyl transferase-mediated dUTP nick end-labeling method. After GalN/LPS injection, nuclear phosphorylated c-Jun levels showed a significant increase, which were attenuated by <b>1</b>. The present findings suggest that luteolin ameliorates d-GalN/LPS-induced liver injury and that this protection is likely due to inhibition of the extrinsic and intrinsic apoptotic pathways.