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首页> 外文期刊>Life sciences >Hydrogen peroxide induced chemokine production in the glia-rich cultured cerebellar granule cells under acidosis.
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Hydrogen peroxide induced chemokine production in the glia-rich cultured cerebellar granule cells under acidosis.

机译：在酸中毒下，过氧化氢诱导富含神经胶质的培养小脑颗粒细胞产生趋化因子。

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摘要

We have documented the time-dependent production of chemotactic cytokine, i.e., IL-8, in the extracellular fluid of astrocyte-rich cultured rat cerebellar granule cells under acidified conditions. In this paper, the mechanism of this production was evaluated based on the production of hydrogen peroxide (H2O2). Significant and time-dependent increases of cytosolic H2O2 were detected under acidosis in astrocyte-rich cultured cell. Upon exposure to 10 microM H2O2, significant levels of IL-8 appeared in the extracellular fluid of astrocyte-rich cells, although an initial transient increase of IL-8 was also seen in the intracellular space. Concurrently, after H2O2 exposure cell injury and a delayed increase of cytosolic Ca2+ levels were detected in astrocyte-rich cells. However, in the absence of extracellular Ca2+, the cell injury and the increase of IL-8 production were significantly attenuated. A synergistic effect of cyclosporine A (an inhibitor of the Ca2+/calmodulin-regulated protein phosphatase) and trifluoperazine (an inhibitor of phospholipase A2) on the suppression of H2O2-induced IL-8 production was clearly evident. These results suggest that extracellular acidosis induced Ca2+-dependent H2O2 production, which in turn stimulated IL-8 expression. which is regulated by the cytosolic Ca2+ cascade. Thus, the production of IL-8 from glia cells may have a role in regulating in the process of cell injury.
机译：我们已经证明了在酸性条件下富含星形胶质细胞培养的大鼠小脑颗粒细胞的细胞外液中趋化性细胞因子，即IL-8的时间依赖性产生。在本文中，基于过氧化氢（H2O2）的产生来评估这种产生的机理。在富含星形胶质细胞的细胞中发生酸中毒时，细胞质中的H2O2显着且随时间增加。暴露于10 microM H2O2后，富含星形胶质细胞的细胞外液中出现了显着水平的IL-8，尽管在细胞内空间中也发现了IL-8的初始瞬时增加。同时，在H2O2暴露后，在富含星形胶质细胞的细胞中检测到细胞损伤和胞质Ca2 +水平的延迟增加。然而，在不存在细胞外Ca 2+的情况下，细胞损伤和IL-8产生的增加被显着减弱。很明显，环孢霉素A（Ca2 + /钙调蛋白调节的蛋白磷酸酶的抑制剂）和三氟拉嗪（磷脂酶A2的抑制剂）对抑制H2O2诱导的IL-8产生了协同作用。这些结果表明细胞外酸中毒诱导了Ca2 +依赖性H2O2的产生，进而刺激了IL-8的表达。这是由胞质Ca2 +级联调节的。因此，由胶质细胞产生的IL-8可能在细胞损伤过程中起调节作用。

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