Liver, Pancreas, and Biliary TractEssential role of tumor necrosis factor α in alcohol-induced liver injury in mice☆,☆☆
Section snippets
Animals
A breeding colony of TNF-R1 knockout mice (p55 −/−) was established at the University of North Carolina at Chapel Hill from breeding pairs kindly donated by Dr. Tak Mak of Amgen Institute (Toronto, Ontario, Canada). Wild-type C57Bl/6J mice and TNF-R2 knockout mice (p75 −/−) were purchased from the Jackson Laboratory (Bar Harbor, ME). Experiments were performed with adult male mice weighing 22-26 g housed in a facility approved by the American Association for Accreditation of Laboratory Animal
Body weights and urine levels of ethanol
Figure 1 shows a typical adult male mouse from this study. All animals survived surgery and gained weight during the subsequent 4 weeks of continuous delivery of the liquid diets with or without ethanol (Table 1). Similar weight gains occurred in wild-type adult mice on chow diet (data not shown), and there were no significant differences in body weights between the groups studied. The reason for the relatively small weight gain observed was that the mice used in this study were adults; similar
Application of continuous enteral alcohol delivery to the mouse
Typical histopathologic findings from livers of wild-type mice fed an ethanol-containing diet indicate that the long-term enteral feeding mouse model is practical. Although surgery in mice is somewhat more difficult than in rats because of their smaller body size, >90% postoperative survival rates can be achieved with care. For optimal survival rates, it was important that the animals be allowed to recover from surgery for 1 week before the liquid diets were initiated. During the recovery
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2022, AquacultureCitation Excerpt :Non-lethal dose of D-GalN/LPS has important clinical significance for animal experiments. Many inflammatory liver illnesses have been linked to TNF-α production in human studies, which involve alcoholic liver disease, viral hepatitis, ischemia/reperfusion liver failure, and immune or drug-induced liver injury (Oreopoulos et al., 2004; Ando et al., 1997; Yin et al., 1999). The release of TNF-α (proinflammatory mediators in hepatocyte apoptosis) is likewise related to the cytotoxicity generated by D-galactosamine/lipopolysaccharide, which may mediate hepatocyte apoptosis or injury (Osawa et al., 2001; Morikawa et al., 1996).
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Address requests for reprints to: Ronald G. Thurman, Ph.D., Department of Pharmacology, Laboratory of Hepatobiology and Toxicology, CB 7365, Mary Ellen Jones Building, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7365. e-mail: [email protected]; fax: (919) 966-1893.
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Supported in part by grants from the National Institute on Alcohol Abuse and Alcoholism.