Non-genomic Effects of Glucocorticoids: An Updated View

被引:190
作者
Panettieri, Reynold A. [1 ]
Schaafsma, Dedmer [2 ]
Amrani, Yassine [3 ]
Koziol-White, Cynthia [1 ]
Ostrom, Rennolds [4 ]
Tliba, Omar [5 ]
机构
[1] Robert Wood Johnson Sch Med, Dept Med, Rutgers Inst Translat Med & Sci, New Brunswick, NJ USA
[2] Sci Impact, Winnipeg, MB R3L 2S9, Canada
[3] Leicester Biomed Res Ctr Resp, Inst Lung Hlth, Dept Infect Immun & Inflammat, Leicester, Leics, England
[4] Chapman Univ, Sch Pharm, Dept Biomed & Pharmaceut Sci, Irvine, CA USA
[5] Long Isl Univ, Coll Vet Med, Dept Biomed Sci, Brookville, NY 11548 USA
基金
美国国家卫生研究院;
关键词
NITRIC-OXIDE SYNTHASE; INTRACELLULAR CA2+; CAVEOLIN ISOFORMS; RECEPTOR; ACTIVATION; DEXAMETHASONE; EXPRESSION; CORTICOSTERONE; MITOCHONDRIA; ALDOSTERONE;
D O I
10.1016/j.tips.2018.11.002
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Glucocorticoid (GC) anti-inflammatory effects generally require a prolonged onset of action and involve genomic processes. Because of the rapidity of some of the GC effects, however, the concept that non-genomic actions may contribute to GC mechanisms of action has arisen. While the mechanisms have not been completely elucidated, the non-genomic effects may play a role in the management of inflammatory diseases. For instance, we recently reported that GCs 'rapidly' enhanced the effects of bronchodilators, agents used in the treatment of allergic asthma. In this review article, we discuss (i) the non-genomic effects of GCs on pathways relevant to the pathogenesis of inflammatory diseases and (ii) the putative role of the membrane GC receptor. Since GC side effects are often considered to be generated through its genomic actions, understanding GC non-genomic effects will help design GCs with a better therapeutic index.
引用
收藏
页码:38 / 49
页数:12
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