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Journal of Ethnopharmacology 2015-Feb

Protective effects of Penthorum chinense Pursh against chronic ethanol-induced liver injury in mice.

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Odkaz sa uloží do schránky
Yi-Wei Cao
Yun Jiang
Da-Yong Zhang
Meng Wang
Wan-Sheng Chen
Huanxing Su
Yi-Tao Wang
Jian-Bo Wan

Kľúčové slová

Abstrakt

BACKGROUND

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.

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.

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