1. S-allylmercaptocysteine reduces carbon tetrachloride-induced hepatic oxidative stress and necroinflammation via nuclear factor kappa B-dependent pathways in mice.
- Author
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Xiao, Jia, Liong, Emily, Ling, Ming-Tat, Ching, Yick-Pang, Fung, Man-Lung, and Tipoe, George
- Subjects
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HEPATOTOXICOLOGY , *LIVER analysis , *ENZYME metabolism , *ANIMAL experimentation , *ANTIOXIDANTS , *BIOPHYSICS , *BLOOD testing , *ENZYME-linked immunosorbent assay , *GARLIC , *HISTOLOGICAL techniques , *INFLAMMATION , *RESEARCH methodology , *LIPID peroxidation (Biology) , *MICE , *NECROSIS , *NITRIC oxide , *POLYMERASE chain reaction , *RESEARCH funding , *STATISTICS , *WESTERN immunoblotting , *PHYTOCHEMICALS , *MALONDIALDEHYDE , *PLANT extracts , *DATA analysis , *OXIDATIVE stress , *ALANINE aminotransferase , *REVERSE transcriptase polymerase chain reaction , *DATA analysis software , *DESCRIPTIVE statistics , *PREVENTION - Abstract
Purpose: To study the protective effects and underlying molecular mechanisms of SAMC on carbon tetrachloride (CCl)-induced acute hepatotoxicity in the mouse model. Methods: Mice were intraperitoneally injected with CCl (50 μl/kg; single dose) to induce acute hepatotoxicity with or without a 2-h pre-treatment of SAMC intraperitoneal injection (200 mg/kg; single dose). After 8 h, the blood serum and liver samples of mice were collected and subjected to measurements of histological and molecular parameters of hepatotoxicity. Results: SAMC reduced CCl-triggered cellular necrosis and inflammation in the liver under histological analysis. Since co-treatment of SAMC and CCl enhanced the expressions of antioxidant enzymes, reduced the nitric oxide (NO)-dependent oxidative stress, and inhibited lipid peroxidation induced by CCl. SAMC played an essential antioxidative role during CCl-induced hepatotoxicity. Administration of SAMC also ameliorated hepatic inflammation induced by CCl via inhibiting the activity of NF-κB subunits p50 and p65, thus reducing the expressions of pro-inflammatory cytokines, mediators, and chemokines, as well as promoting pro-regenerative factors at both transcriptional and translational levels. Conclusions: Our results indicate that SAMC mitigates cellular damage, oxidative stress, and inflammation in CCl-induced acute hepatotoxicity mouse model through regulation of NF-κB. Garlic or garlic derivatives may therefore be a potential food supplement in the prevention of liver damage. [ABSTRACT FROM AUTHOR]
- Published
- 2012
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