| ironjustice@aol.com 2006-09-19, 9:32 pm |
| Increased iron deposition in rat liver fibrosis induced by a
high-dose injection of dimethylnitrosamine.
Guo L, Enzan H, Hayashi Y, Miyazaki E, Jin Y, Toi M, Kuroda N, Hiroi M
Exp Mol Pathol. 2006 Sep 14;
Using a developed rat model of hepatic necrosis and subsequent fibrosis
induced by a high-dose intraperitoneal injection of dimethylnitrosamine
(DMN), we studied iron deposition and expression of transforming growth
factor-beta(1) (TGF-beta(1)) during the development of persistent liver
fibrosis. Rats were sacrificed at several timepoints from 6 h to 10
months post-injection and the livers were examined for iron content and
distribution, and for expression of alpha-smooth muscle actin, ED-1,
TGF-beta(1), and collagen (alpha(2))I. Morphologic evidence of acute
submassive hemorrhagic necrosis peaked at 36 h; on day 3 the residual
parenchyma contained activated hepatic stellate cells (HSCs) and
necrotic areas contained numerous macrophages; and on day 5, necrotic
tissues and erythrocytes had been phagocytosed and macrophages
contained abundant iron deposits. From days 7 to 10, iron-laden
macrophages and activated HSCs (myofibroblasts) populated the fibrous
septa in parallel. From week 2 to month 10, closely arranged
macrophages and myofibroblasts were found in central-to-central
bridging fibrotic tissue. TGF-beta(1) was strongly detected in both
macrophages and HSCs during development of liver fibrosis. Our data
suggest that increased iron deposition may be involved in the
initiation and perpetuation of rat liver fibrosis. Iron-laden
macrophages may influence HSCs through the action of TGF-beta(1) in
DMN-induced liver fibrosis.
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