| Autor: |
Lee, Clair M., Knight, Belinda, Yeoh, George C., Ramm, Grant A., Olynyk, John K. |
| Předmět: |
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| Zdroj: |
Journal of Gastroenterology & Hepatology; Nov2005, Vol. 20 Issue 11, p1762-1768, 7p, 6 Diagrams, 1 Chart |
| Abstrakt: |
Background and Aims: Lymphotoxin-β (LT-β) may play a role in the pathogenesis of chronic liver injury. The aim of this study was to determine in an animal model of bile duct ligation liver injury whether LT-β expression is induced and whether Kupffer cells are an intrahepatic source of LT-β. Methods: Sprague–Dawley rats were divided into two groups: one group received a single dose of GdCl (a Kupffer cell-blocking agent, 10 mg/kg i.v.), whereas the other group received saline. One day later, the groups underwent bile duct ligation or a sham operation. Liver tissue was obtained on days 1, 3, 5, and 8 for assessment of Kupffer cell numbers, early fibrogenic events and LT-β gene expression. Kupffer cells were isolated using pronase/collagenase perfusion and centrifugal elutriation. Results: Hepatic LT-β mRNA expression increased early following bile duct ligation. Pretreatment of bile duct-ligated animals with GdCl significantly reduced the number of Kupffer cells, delayed the rise in LT-β expression, but had no effect on fibrogenesis. Recovery of the Kupffer cell population in these animals was accompanied by increased hepatic LT-β expression. The LT-β ligand and receptor were expressed by isolated normal Kupffer cells. Conclusions: Hepatic LT-β expression is induced early following bile duct ligation. Kupffer cells may be an intrahepatic source of LT-β. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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