Volume 161, 23 February 2015, Pages 92–98
Research Paper
Protective effects of Penthorum chinense Pursh against chronic ethanol-induced liver injury in mice
Abstract
Ethnopharmacological relevance
Penthorum chinense
Pursh (Penthoraceae) has been used as a Miao ethnomedicine for the
treatment of jaundice, cholecystitis, edema, infectious hepatitis and
anti-drunk hangover in China. The aim of present study is to investigate
the possible protective effects of Penthorum chinense against chronic ethanol-induced liver injury.
Material and methods
Mice
were fed a Lieber-DeCarli liquid diet containing alcohol or isocaloric
maltose dextrin as control diet with or without aqueous extract of Penthorum chinense
(PCP, 5.15 and 10.30 g/kg/BW) for 4 weeks. Silymarin (86 mg/kg) was
used as positive control to compare the efficacy of PCP against chronic
ethanol-induced hepatotoxicity.
Results
Treatment
with PCP (10.30 g/kg) significantly reduced the increases in serum ALT
and AST levels, hepatic lipid accumulation and inflammatory cytokines (i.e.
TNF-α, IL-6), which were induced by chronic ethanol exposure. PCP was
also found to attenuate reactive oxygen species (ROS) generation and
malondialdehyde (MDA) level, restore the glutathione (GSH) depletion,
and increase the superoxide dismutase (SOD) and glutathione peroxidase
(GPx) activities. In addition, PCP supplementation (10.30 g/kg)
inhibited the induction of hepatic cytochrome P450 2E1 (CYP2E1), a major
contributor to ethanol-mediated oxidative stress, and up-regulated the
expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and its
downstream anti-oxidant protein heme oxygenase-1 (HO-1) in
ethanol-treated mice.
Conclusions
These results indicate that the co-treatment with aqueous extract of Penthorum chinense
(10.30 g/kg) protects against chronic ethanol-induced liver injury,
possibly through suppressing CYP2E1-mediated oxidative stress and
enhancing the oxidant defense systems via the activation of Nrf2/HO-1 pathway.
Keywords
- Penthorum chinense Pursh;
- Alcoholic liver disease;
- Ethanol-induced liver injury;
- Oxidative stress;
- Oxidant defense system
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