Dexamethasone and hydrogen peroxide production by mesangial cells during phagocytosis.
Dexamethasone and hydrogen peroxide production by mesangial cells during phagocytosis.
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系膜细胞在吞噬作用过程中产生地塞米松和过氧化氢。
DOI：
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发表时间：
1986
影响因子：
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通讯作者：
R. Ardaillou
中科院分区：
文献类型：
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作者：
L. Baud;J. Pérez;R. Ardaillou
我们之前已经证明，高比例的大鼠培养的肾小球系膜细胞吞噬血清处理的酵母聚糖（STZ）（L. Baud，J. Hagege，J. Sraer，E. Rondeau，J. Perez，和 R. Ardaillou，J. Exp. Med. 158：1836-1852，1983）。吞噬作用刺激花生四烯酸代谢并产生 H2O2。将系膜细胞暴露于地塞米松 48 小时，吞噬作用诱导的 H2O2 产生量呈剂量依赖性下降，50% 抑制浓度为 32 nM。 H2O2 释放的减少与前列腺素 (PG) E2 产生的抑制有关。地塞米松的作用可以被认为是由于受体介导的蛋白质合成调节所致，因为地塞米松不会立即发挥作用，而是在3小时的滞后期后才发挥作用； RU 38486 是地塞米松受体的有力竞争者，可以抵消 H2O2 生成的减少；放线菌素和放线菌酮均减弱地塞米松的抑制作用。用地塞米松预处理系膜细胞也会导致细胞吞噬能力出现剂量依赖性下降（1 µM 地塞米松抑制 63%）。然而，无论吞噬作用是否被细胞松弛素 B 阻断，地塞米松对以对照百分比表示的 H2O2 产生的抑制作用相似。这一结果以及地塞米松抑制由可溶性刺激（A 23187 离子载体，PAF）触发的细胞中 H2O2 产生的事实表明，地塞米松对 H2O2 产生的影响独立于对 H2O2 产生的影响。吞噬作用。仅当地塞米松转化为 PGE2 被吲哚美辛抑制时，添加外源花生四烯酸才会降低地塞米松的作用。（摘要截断为 250 字）
We have previously demonstrated that a high percentage of rat cultured mesangial cells phagocytized serum-treated zymosan (STZ) (L. Baud, J. Hagege, J. Sraer, E. Rondeau, J. Perez, and R. Ardaillou, J. Exp. Med. 158: 1836-1852, 1983). Phagocytosis resulted in stimulation of arachidonic acid metabolism with generation of H2O2. Exposure of mesangial cells to dexamethasone for 48 h produced a dose-dependent decrease in phagocytosis-induced production of H2O2 with a 50% inhibitory concentration of 32 nM. The decrease in H2O2 release was associated with the inhibition of prostaglandin (PG) E2 production. The effect of dexamethasone could be considered as due to receptor-mediated modulation of protein synthesis since dexamethasone was not active immediately but only after a lag period of 3 h; RU 38486, a potent competitor for dexamethasone receptors, counteracted the reduction in H2O2 generation; and actinomycin and cycloheximide both blunted the inhibitory effect of dexamethasone. Pretreatment of mesangial cells with dexamethasone also produced a dose-dependent decrease in the phagocytic capability of the cells (63% inhibition for 1 microM dexamethasone). However, the inhibitory effect of dexamethasone on H2O2 production expressed as percentage of control was similar whether or not phagocytosis had been blocked by cytochalasin B. This result and also the fact that dexamethasone inhibited H2O2 production in cells triggered with soluble stimuli (A 23187 ionophore, PAF) suggested that the effect of dexamethasone on H2O2 generation was independent of that on phagocytosis. Addition of exogenous arachidonic acid reduced the effect of dexamethasone only when its conversion into PGE2 was inhibited by indomethacin.(ABSTRACT TRUNCATED AT 250 WORDS)