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Effects of Glucocorticoids on Apoptosis and Clearance of Apoptotic Cells

机译:糖皮质激素对凋亡细胞凋亡和间隙的影响

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摘要

The glucocorticoid (GC) drugs are one of the most commonly prescribed and effective anti-inflammatory agents used for the treatment of many inflammatory disorders through their ability to attenuate phlogistic responses. The glucocorticoid receptor (GCR) primarily mediates GC actions via activation or repression of gene expression. GCs directly induce the expression of proteins displaying anti-inflammatory activities. However, the likely predominant effect of GCs is the repression of multiple inflammatory genes that invariably are overexpressed during nonresolving chronic inflammation. Although most GC actions are mediated through regulation of transcription, rapid nongenomic actions have also been reported. In addition, GCs modulate inflammatory cell survival, inducing apoptosis in immature thymocytes and eosinophils, while delaying constitutive neutrophil apoptosis. Importantly, GCs promote noninflammatory phagocytosis of apoptotic cell targets, a process important for the successful resolution of inflammation. Here, the effects and mechanisms of action of GC on inflammatory cell apoptosis and phagocytosis will be discussed.
机译:糖皮质激素(GC)药物是用于通过衰减磷酸性反应的能力治疗许多炎症疾病的最常用和有效的抗炎剂之一。糖皮质激素受体(GCR)主要通过激活或抑制基因表达来介导GC作用。 GCS直接诱导蛋白质表达显示抗炎活动。然而,GCS的可能主要效果是抑制多种炎症基因,其在非溶解慢性炎症期间总体抑制。虽然大多数GC措施是通过转录的调节介导的,但也已经报道了快速的不良组。此外,GCS调节炎症细胞存活,诱导肾小球细胞和嗜酸性粒细胞的细胞凋亡,同时延迟组成型中性粒细胞凋亡。重要的是,GCS促进凋亡细胞靶标的非炎症性吞噬作用,这是对炎症成功分离的过程。在此,将讨论GC对炎症细胞凋亡和吞噬作用的影响和机制。

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