Brandwein S R, Sipe J D, Skinner M, Cohen A S
J Rheumatol. 1985 Jun;12(3):418-26.
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.
研究了全身给予前列腺素E1(PGE1)在硝酸银慢性刺激诱导的实验性CBA/J小鼠淀粉样变性中的抗炎活性。PGE1降低了脾脏中淀粉样蛋白A(AA)的沉积(p = 0.035)。急性期PGE1未抑制血清淀粉样蛋白A(SAA)水平,而无论是否进行PGE1治疗,SAA水平降低似乎是慢性炎症期的一个组成部分。淀粉样增强因子(AEF)诱导的加速淀粉样沉积未被PGE1阻断。这表明PGE1在淀粉样蛋白沉积前期抑制淀粉样变性,可能是通过阻止AEF或其他沉积因子的形成。