Administration of prostaglandin E1 analog reduces rat hepatic and ito cell collagen gene expression and collagen accumulation after bile duct ligation injury
✍ Scribed by David W. A. Beno; Ronald Espinal; Brian M. Edelstein; Bernard H. Davis
- Publisher
- John Wiley and Sons
- Year
- 1993
- Tongue
- English
- Weight
- 1012 KB
- Volume
- 17
- Category
- Article
- ISSN
- 0270-9139
No coin nor oath required. For personal study only.
✦ Synopsis
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 i d w y induced by bile duct ligation. Enisoprost, a prostaglandin El 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-& Overall liver inflammation and cell proliferation were not altered, suggesting that prostaglandin E acts distal to the initial injurious event($. During later phases, drug administration reduced total collagen accumulation and type I collagen periductular idltration associated with early nodule formation. (HEPATOLOGY 1993;17:707-714.)
Recent in uiuo studies suggest that prostaglandin E (PGE) compounds may have significant immunosuppressive properties (1). Clinical utility may relate to PGE interference with the lymphocyte interleukin (1L)-2 receptor, but the precise underlying mechanismb) of action remains to be determined (2). In uitro,studies have found that PGE may differentially modulate cytokine responsiveness; PGE, suppresses both IL-1 and IL-2-induced mitogenesis, whereas PGE, only alters the IL-2 response (2-5).
The potential therapeutic usefulness of PGE compounds in nonimmunological models of tissue injury and fibrosis is poorly understood, but increasing evidence