Authors: | Fujita, J.; Marino, M. W.; Wada, H.; Jungbluth, A. A.; Mackrell, P. J.; Rivadeneira, D. E.; Stapleton, P. P.; Daly, J. M. |
Article Title: | Effect of TNF gene depletion on liver regeneration after partial hepatectomy in mice |
Abstract: | Background. Tumor necrosis factor-alpha (TNF) is thought to art as a stimutlator for initiating hepalocyte proliferation after partial hepatetectomy (PH). At the same time TNF induces a series of inflammatory responses that may Be detrimental for the liver and other remote organs. The purpose of this study runs to investigate the effect of TNF on the pathophysiologic state after PH. Methods. Wild-type (TNF+/+) and TNF-deficient (TNF-/-) mice underwent 70% PH. Hepatocyte proliferation was assessed by bromodeoxyuridine labeling and mitotic index. Liver function was evaluated by alanine aminotransferase (ALT) and total bilirubin levels in serum after PH. Myeloperoxidase activity in the liver and lung was measured as a marker for neutrophil activation. Results. No differences were observed in liver regeneration or hepatocyle proliferation between TNF+/+ and TNF-/- mice The survival of TNF-/- mice on day I after PH was significantly higher than that of TNF+/+ mice, but both groups had similar survival thereafter The ALT level was significantly higher in TNF+/+ mice 6 hours after PH and myeloiproxidase activities in both liver and lung were markedly elevated in TNF+/+ mice compared with TNF-/- mice. Conclusions. These findings demonstrate that TNF gene-depleted mice do not demonstrate delayed liver regeneration but no suppress neutrophil activation after PH compared with results in wild-type (TNF+/+) mice. |
Keywords: | apoptosis; rat; receptor; injury; failure; tumor-necrosis-factor; factor-alpha; growth; endotoxin |
Journal Title: | Surgery |
Volume: | 129 |
Issue: | 1 |
ISSN: | 0039-6060 |
Publisher: | Elsevier Inc. |
Date Published: | 2001-01-01 |
Start Page: | 48 |
End Page: | 54 |
Language: | English |
ACCESSION: | WOS:000166396500007 |
DOI: | 10.1067/msy.2001.109120 |
PROVIDER: | wos |
PUBMED: | 11150033 |
Notes: | Article -- Source: Wos |