Abstract
The protective effects of interleukin-22 (IL-22) on acute alcohol-induced liver injury were investigated. Mice were gavaged with 7 doses of alcohol (56% wt/vol, 15.2 mL/kg of body weight for each dose) over the 24 h, and IL-22 (0.5 mg/kg BW) was given to the mice by injection into the tail vein 1 h after alcohol administration. The results indicated that acute alcohol administration caused prominent hepatic microvesicular steatosis and an elevation of serum transaminase activities, induced a significant decrease in hepatic glutathione in conjunction with enhanced lipid peroxidation, and increased hepatocyte apoptosis as well as hepatic TNF-alpha production. IL-22 treatment attenuated these adverse changes induced by acute alcohol administration. The protective effects of IL-22 on alcohol-induced hepatotoxicity were due mainly to its anti-inflammatory, anti-oxidant, and anti-apoptotic features.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Alanine Transaminase / blood
-
Alanine Transaminase / drug effects
-
Alanine Transaminase / metabolism
-
Animals
-
Antioxidants / metabolism
-
Apoptosis / drug effects
-
Ethanol / toxicity*
-
Fatty Liver, Alcoholic / etiology
-
Fatty Liver, Alcoholic / metabolism
-
Fatty Liver, Alcoholic / pathology
-
Fatty Liver, Alcoholic / prevention & control*
-
Glutathione / drug effects
-
Glutathione / metabolism
-
Hepatitis, Alcoholic / etiology
-
Hepatitis, Alcoholic / metabolism
-
Hepatitis, Alcoholic / pathology
-
Hepatitis, Alcoholic / prevention & control*
-
Inflammation
-
Interleukin-22
-
Interleukins / administration & dosage*
-
Lipid Peroxidation / drug effects
-
Liver / cytology
-
Liver / drug effects
-
Liver / metabolism
-
Liver / pathology*
-
Male
-
Mice
-
Tumor Necrosis Factor-alpha / drug effects*
-
Tumor Necrosis Factor-alpha / metabolism
Substances
-
Antioxidants
-
Interleukins
-
Tumor Necrosis Factor-alpha
-
Ethanol
-
Alanine Transaminase
-
Glutathione