Luteolin and luteolin-7-O-glucoside protect against acute liver injury through regulation of inflammatory mediators and antioxidative enzymes in GalN/LPS-induced hepatitic ICR mice
10.4162/nrp.2019.13.6.473
- Author:
Chung Mu PARK
1
;
Young Sun SONG
Author Information
1. Department of Clinical Laboratory Science, Dong-Eui University, Busan 47340, Korea.
- Publication Type:Original Article
- Keywords:
Luteolin;
Luteolin-7-O-glucoside;
Inflammation;
NF-kappa B;
NF-E2-Related Factor 2
- MeSH:
Animals;
Galactosamine;
Hepatitis;
Humans;
Inflammation;
Injections, Intraperitoneal;
Liver;
Luteolin;
Male;
Mice;
Mice, Inbred ICR;
NF-E2-Related Factor 2;
NF-kappa B;
Prostaglandin-Endoperoxide Synthases;
Transcription Factors
- From:Nutrition Research and Practice
2019;13(6):473-479
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND/OBJECTIVES: Anti-inflammatory and antioxidative activities of luteolin and luteolin-7-O-glucoside were compared in galactosamine (GalN)/lipopolysaccharide (LPS)-induced hepatitic ICR mice. MATERIALS/METHODS: Male ICR mice (6 weeks old) were divided into 4 groups: normal control, GalN/LPS, luteolin, and luteolin-7-O-glucoside groups. The latter two groups were administered luteolin or luteolin-7-O-glucoside (50 mg/kg BW) daily by gavage for 3 weeks after which hepatitis was induced by intraperitoneal injection of GalN and LPS (1 g/kg BW and 10 µg/kg BW, respectively). RESULTS: GalN/LPS produced acute hepatic injury by a sharp increase in serum AST, ALT, and TNF-α levels, increases that were ameliorated in the experimental groups. In addition, markedly increased expressions of cyclooxygenase (COX)-2 and its transcription factors, nuclear factor (NF)-κB and activator protein (AP)-1, were also significantly attenuated in the experimental groups. Compared to luteolin-7-O-glucoside, luteolin more potently ameliorated the levels of inflammatory mediators. Phase II enzymes levels and NF-E2 p45-related factor (Nrf)-2 activation that were decreased by GalN/LPS were increased by luteolin and luteolin-7-O-glucoside administration. In addition, compared to luteolin, luteolin-7-O-glucoside acted as a more potent inducer of changes in phase II enzymes. Liver histopathology results were consistent with the mediator and enzyme results. CONCLUSION: Luteolin and luteolin-7-O-glucoside protect against GalN/LPS-induced hepatotoxicity through the regulation of inflammatory mediators and phase II enzymes.
