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首页> 外文期刊>Cellular Physiology and Biochemistry >The Glucocorticoid Dexamethasone Inhibits U937 Cell Adhesion and Neutrophil Release via RhoA/ROCK1-Dependent and Independent Pathways
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The Glucocorticoid Dexamethasone Inhibits U937 Cell Adhesion and Neutrophil Release via RhoA/ROCK1-Dependent and Independent Pathways

机译：糖皮质激素地塞米松通过RhoA / ROCK1依赖性和独立途径抑制U937细胞粘附和中性粒细胞释放

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biAims /i/bThe aim of the present study was to investigate the role of the Ras homolog family member A (RhoA)/Rho-associated coiled-coil-containing protein kinase 1 (ROCK1) signaling pathway in the inhibition of inflammatory responses by the glucocorticoid dexamethasone (Dex). biMethods /i/bThe inhibitory effects of Dex and Rho-kinase inhibitor fasudil (Fas) on phorbol ester-induced release of Osub2/subsup-/sup and MPO from neutrophils and on U937 mononuclear cell adhesion were examined along with the expression and activity levels of RhoA and ROCK1. biResults /i/bHigh doses of Dex rapidly inhibited the release of Osub2/subsup-/sup and myeloperoxidase (MPO) from neutrophils and the adhesion of U937 cells, while Fas was only found to inhibit U937 cell adhesion. Additionally, Dex suppressed ROCK1 activity. However, Dex had no effects on ROCK1 or RhoA expression levels or on RhoA activity. Neither the glucocorticoid receptor antagonist mifepristone (RU-486) nor the protein synthesis inhibitor cycloheximide (CHX) was able to suppress the effects of Dex (p0.05). biConclusions /i/bThe present findings indicate that Dex suppressed neutrophil release through ROCK1-independent mechanisms and inhibited the adhesion of U937 mononuclear cells through ROCK1-dependent non-genomic mechanisms that did not involve RhoA.
机译：目标 本研究的目的是研究Ras同源家族成员A（RhoA）/ Rho相关的含卷曲螺旋蛋白激酶1（ROCK1 ）糖皮质激素地塞米松（Dex）抑制炎症反应的信号通路。 方法 Dex和Rho激酶抑制剂fasudil（Fas）对佛波酯诱导的O 2 -<检测中性粒细胞的MPO以及U937单核细胞的粘附情况，以及RhoA和ROCK1的表达和活性水平。 结果 高剂量的Dex迅速抑制中性粒细胞和中性粒细胞释放O 2 -和髓过氧化物酶（MPO）。 U937细胞粘附，而Fas仅被发现抑制U937细胞粘附。此外，Dex抑制了ROCK1的活性。但是，Dex对ROCK1或RhoA表达水平或RhoA活性没有影响。糖皮质激素受体拮抗剂米非司酮（RU-486）或蛋白质合成抑制剂环己酰亚胺（CHX）均不能抑制Dex的作用（p> 0.05）。 结论 本研究结果表明Dex通过ROCK1依赖性机制抑制嗜中性粒细胞释放，并通过不涉及RhoA的ROCK1依赖性非基因机制抑制U937单个核细胞的粘附。 。

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