Administration of prostaglandin E1 analog reduces rat hepatic and ito cell collagen gene expression and collagen accumulation after bile duct ligation injury

Abstract

Recent studies suggest that prostaglandin E may have the ability to suppress cytokine responsiveness. We examined the effects of prostaglandin E administration on several parameters of acute and chronic liver injury induced by bile duct ligation. Enisoprost, a prostaglandin E1 analog, was found to suppress early hepatic and Ito cell type I collagen gene expression without diminishing the induction of the fibrogenic cytokine transforming growth factor-beta. Overall liver inflammation and cell proliferation were not altered, suggesting that prostaglandin E acts distal to the initial injurious event(s). During later phases, drug administration reduced total collagen accumulation and type I collagen periductular infiltration associated with early nodule formation.

Interferon gamma decreases hepatic stellate cell activation and extracellular matrix deposition in rat liver fibrosis

“…34,35 Desmin staining appears as a useful marker for rat HSC under different experimental con-sis. [1][2][3][4] This method has proven, in other studies [67][68] as well as ours, 13 a simple and reproducible technique to ditions, 8,9,19,46 although other markers for normal 63 or activated 36 HSC have recently been proposed. quantitate collagen in liver sections.…”

Normal and Pathologic Soft Tissue Remodeling: Role of the Myofibroblast, with Special Emphasis on Liver and Kidney Fibrosis

“…Isolated hepatic stellate cells respond to norepinephrine by increasing their secretion of prostaglandins (Athari et al, 1994). Prostaglandins decrease the proliferation of activated hepatic stellate cells (Mallat et al, 1996), and prostaglandin E1 treatment decreases liver fibrosis in the bile duct ligation model (Beno et al, 1993). One could thus conclude that catecholamines may have a protective effect against fibrogenesis.…”

Role of NF-κB in the Antiproliferative Effect of Endothelin-1 and Tumor Necrosis Factor-α in Human Hepatic Stellate Cells

“…For example, monocyte chemotactic protein-1 or intercellular adhesion molecule 1 are expressed in rat HSC and up-regulated by TNF-␣ (55, 56); however, TNF-␣ is mitogenic for rat HSC (30). On the other hand, prostaglandins E are antifibrogenic in an in vivo model of liver fibrosis (57), and in vitro studies show that in rat HSC, prostaglandins E inhibit both collagen I production (57) and cell proliferation (58). These findings, together with the fact that ET-1 and TNF-␣ inhibit the growth of human myofibroblastic HSC, following NF-B-dependent COX-2 induction, would be in favor of a negative regulatory role of this pathway in liver fibrogenesis.…”