Prostaglandin E1 inhibition of experimental amyloidosis in CBA/J mice.
The antiinflammatory activity of systemically administered prostaglandin E1 (PGE1) was studied in experimental CBA/J mouse amyloidosis induced by chronic stimulation with silver nitrate. PGE1 lowered splenic deposition of amyloid A protein (AA) (p = 0.035). Serum amyloid A protein (SAA) levels were not suppressed by PGE1 in the acute phase, while decreased SAA levels appeared to be an integral part of the chronic inflammatory phase, with or without PGE1 treatment. Accelerated amyloid deposition induced by amyloid-enhancing factor (AEF) was not blocked by PGE1. This suggests that PGE1 inhibits amyloidosis in the predeposition phase, possibly by preventing formation of AEF or other deposition factors.
D000527:Alprostadil / Q000494:pharmacology*; D000686:Amyloidosis / Q000139:chemically induced / Q000378:metabolism / Q000517:prevention & control*; D000818:Animals; D000893:Anti-Inflammatory Agents; D005260:Female; D006023:Glycoproteins / Q000096:biosynthesis / Q000494:pharmacology; D051379:Mice; D008808:Mice, Inbred CBA; D000685:Serum Amyloid A Protein / Q000378:metabolism; D012835:Silver Nitrate; D013154:Spleen / Q000378:metabolism; D013997:Time Factors
D000893:Anti-Inflammatory Agents; D006023:Glycoproteins; D000685:Serum Amyloid A Protein; C046748:amyloid enhancing factor; D012835:Silver Nitrate; D000527:Alprostadil