Podjarny E, Rathaus M, Pomeranz A, Shapira J, Bernheim J
Department of Nephrology, Meir Hospital, Kfar-Saba and Sackler School of Medicine, Tel-Aviv University, Israel.
Nephron. 1989;53(1):50-3. doi: 10.1159/000185701.
Activation of macrophages and release of mediators that activate the coagulation system characterize proliferative glomerulonephritis. To evaluate the possible role of prostanoids in this process, isolated rat glomeruli (G) and peritoneal macrophages (M) or a combination of the two (G + M) were incubated in the presence of thrombin (2 U/ml). In G, thrombin inhibited only the synthesis of thromboxane B2. In M and G + M incubations, the synthesis of prostaglandin I2 and thromboxane A2 was inhibited by thrombin. This effect was abolished by the addition of arachidonic acid. As prostanoids may play a modulatory role in the interaction between macrophages and glomerular cells, inhibition of their synthesis by thrombin might enhance macrophage activity.
巨噬细胞的激活以及激活凝血系统的介质释放是增殖性肾小球肾炎的特征。为了评估前列腺素类物质在此过程中可能发挥的作用，将分离的大鼠肾小球（G）和腹膜巨噬细胞（M）或二者的组合（G + M）在凝血酶（2 U/ml）存在的情况下进行孵育。在肾小球中，凝血酶仅抑制血栓素B2的合成。在巨噬细胞以及肾小球与巨噬细胞组合的孵育体系中，凝血酶抑制前列腺素I2和血栓素A2的合成。添加花生四烯酸可消除这种作用。由于前列腺素类物质可能在巨噬细胞与肾小球细胞之间的相互作用中起调节作用，凝血酶对其合成的抑制可能会增强巨噬细胞的活性。
