Basic–Liver, Pancreas, and Biliary TractThalidomide prevents alcoholic liver injury in rats through suppression of Kupffer cell sensitization and TNF-α production☆
Section snippets
Animals and treatments
In this study, a model of alcoholic liver injury based on the sensitization of Kupffer cells, in which rats are given ethanol (5 g/kg body weight) once every 24 hours,22 was used. This model achieves inflammatory and necrotic changes in the liver only in 8 weeks, which mimics features of clinical alcohol liver injury.22 Liver damage was evaluated after 8 weeks of treatment with ethanol because histologic manifestations are preceded by sensitization of Kupffer cells to LPS treatment, and Kupffer
Effect of thalidomide on alcoholic liver injury
There were no differences in body weight growth among the control, thalidomide, ethanol, and ethanol plus thalidomide groups during 8 weeks of ethanol treatment. All rats survived for 8 weeks. Animals treated with thalidomide only showed completely normal liver histology (Figure 1B).
Thalidomide prevents alcohol-induced liver injury
In this study, we used a model of alcohol-induced liver injury based on sensitization of Kupffer cells22 because it has been established that sensitization of Kupffer cells to LPS and consequent overproduction of TNF-α play a central role in the pathogenesis of alcohol liver disease.1, 2, 31 This model makes it possible to achieve pathologic changes in the liver (e.g., steatosis, inflammation, and necrosis) that resemble alterations that occur in the enteral-feeding model without surgery (
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Address requests for reprints to: Nobuhiro Sato, M.D., Department of Gastroenterology, Juntendo University School of Medicine, 2-1-1, Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan. e-mail: [email protected]; fax: (81) 3-3813-8862.