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1 Laboratory of Hepatobiology and Toxicology, Department of Pharmacology and Departments of 2 Surgery and 3 Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599; 4 Department of Physiology and Pharmacology, School of Medicine, Oregon Health Sciences University, Portland, Oregon 97201-3098; and 5 Bayer Pharmaceuticals, D-42285 Wuppertal, Germany
The role of
Kupffer cells in CCl4-induced fibrosis was investigated in
vivo. Male Wistar rats were treated with phenobarbital and
CCl4 for 9 wk, and a group of rats were injected with the Kupffer cell toxicant gadolinium chloride (GdCl3) or were
fed glycine, which inactivates Kupffer cells. After CCl4
alone, the fibrosis score was 3.0 ± 0.1 and collagen protein
and mRNA expression were elevated, but GdCl3 or glycine
blunted these parameters. Glycine did not alter cytochrome
P-450 2E1, making it unlikely that glycine affects
CCl4 metabolism. Treatment with GdCl3
or glycine prevented CCl4-induced increases in transforming
growth factor (TGF)-
1 protein levels and expression.
CCl4 treatment increased 
-smooth muscle actin staining
(score 3.0 ± 0.2), whereas treatment with GdCl3 and
glycine during CCl4 exposure blocked this effect (1.2 ± 0.5); there was no staining with glycine treatment. These results
support previous in vitro data and demonstrate that treatment of rats
with the selective Kupffer cell toxicant GdCl3 prevents
stellate cell activation and the development of fibrosis.
Kupffer cells; transforming growth factor-; rat; -smooth
muscle actin; 1(I) collagen
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