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Protein synthesis dependent effects of kinins on astrocyte prostaglandin synthesis.

机译:激肽对星形胶质细胞前列腺素合成的蛋白质合成依赖性作用。

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It has been shown that kinins and their receptors are over expressed in the brain under pathophysiological conditions such as inflammation. However, little is known about the possible role of kinins, and especially bradykinin in brain inflammation. Although kinins are thought to have immediate effects, peptides may also exert longer and protein synthesis dependent actions. To evaluate this possibility, we assessed the regulation of prostaglandin E(2) synthesis after 15h bradykinin or Lys-des-Arg(9)-bradykinin (B(1) receptor agonist) treatment in rat neonatal astrocytes. Bradykinin, dose dependently stimulated basal and lipopolysaccharide-induced prostaglandin E(2) production, whereas exposure of astrocytes to the B(1) receptor agonist decreased both basal and lipopolysaccharide-induced prostaglandin E(2) release in a dose-dependent manner. These kinin effects on PGE(2) synthesis were completely abrogated by actinomycin-D and cycloheximide, suggesting de novo synthesis of proteins. Bradykinin also increased cyclooxygenase-2 protein levels about 2-fold, while the B(1) receptor agonist decreased cyclooxygenase-2 protein expression. There was no change in cyclooxygenase-1 protein levels after treatment with either of the kinins. Our data suggest a delayed feedback regulatory mechanism of kinins on astrocyte inflammation, whereby astrocyte prostaglandin synthesis is initially enhanced by bradykinin (B(2)) and eventually blocked by kinin breakdown product, acting on B(1) receptors. At least part of this presumed feedback loop could be mediated by de novo protein synthesis of cyclooxygenase-2.
机译:已经表明,在诸如炎症的病理生理条件下,激肽及其受体在脑中过度表达。然而,人们对激肽尤其是缓激肽在脑部炎症中的可能作用了解甚少。尽管激肽被认为具有立竿见影的效果,但肽也可能发挥更长的作用,并依赖蛋白质合成。为了评估这种可能性,我们评估了大鼠新生星形胶质细胞中15h缓激肽或Lys-des-Arg(9)-缓激肽(B(1)受体激动剂)治疗后前列腺素E(2)的合成。缓激肽以剂量依赖性方式刺激基础和脂多糖诱导的前列腺素E(2)的产生,而星形胶质细胞暴露于B(1)受体激动剂则以剂量依赖性方式降低了基础和脂多糖诱导的前列腺素E(2)的释放。这些激肽对PGE(2)合成的影响已被放线菌素D和环己酰亚胺完全废止,表明从头合成了蛋白质。缓激肽还增加了环氧合酶2蛋白水平约2倍,而B(1)受体激动剂则降低了环氧合酶2蛋白的表达。用任何一种激肽处理后,环氧合酶-1的蛋白水平均没有变化。我们的数据表明,激肽对星形胶质细胞炎症的延迟反馈调节机制,从而星形胶质细胞前列腺素的合成最初由缓激肽(B(2))增强,并最终由激肽分解产物阻断,作用于B(1)受体。该推测的反馈回路的至少一部分可以由环氧合酶-2的从头蛋白质合成介导。

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