1. Tetramethylpyrazine protects mice against thioacetamide-induced acute hepatotoxicity
- Author
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Sheng-Chou C Tasi, Chi-Feng Liu, Edmund Cheung So, Kar-Lok Wong, and Tian-Chyuan Huang
- Subjects
Interleukin 2 ,Male ,Endocrinology, Diabetes and Metabolism ,Clinical Biochemistry ,Pharmacology ,Thioacetamide ,medicine.disease_cause ,Lipid peroxidation ,chemistry.chemical_compound ,Mice ,medicine ,Tetramethylpyrazine ,Animals ,Pharmacology (medical) ,Aspartate Aminotransferases ,Molecular Biology ,Chromatography, High Pressure Liquid ,Mice, Inbred ICR ,Biochemistry (medical) ,Alanine Transaminase ,Cell Biology ,General Medicine ,Malondialdehyde ,digestive system diseases ,In vitro ,chemistry ,Biochemistry ,Liver ,Pyrazines ,Interleukin-2 ,Hepatocellular injury ,Lipid Peroxidation ,Chemical and Drug Induced Liver Injury ,Oxidative stress ,medicine.drug - Abstract
In this study, the intraperitoneal administration of 1 mg/kg thioacetamide (TAA) produced hepatotoxicity in mice. The increase in serum SGOT and SGPT produced at 24 h by this regimen was decreased in a dose-dependent manner by coadministration of tetramethylpyrazine (TMP; 10, 25 and 50 mg/kg). A rise in serum interleukin-2 was similarly prevented. Increased concentrations of malondialdehyde (MDA) generated in vitro in liver homogenates prepared from TAA-treated mice were decreased by TMP treatments. The increase in MDA produced by TAA was also prevented by in vitro addition of TMP to liver homogenates. These results suggest that part of the hepatocellular injury induced by TAA is mediated by oxidative stress caused by the action of cytokines through lipid peroxidation. TMP appears to act by preventing lipid peroxidation.
- Published
- 2002