期刊
MOLECULAR AND CELLULAR ENDOCRINOLOGY
卷 301, 期 1-2, 页码 123-131出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2008.09.031
关键词
Glucocorticoid; 11 beta-Hydroxysteroid dehydrogenase; Macrophage; Mast cell; Inflammation; Arthritis
资金
- MRC [G0800235] Funding Source: UKRI
- Medical Research Council [G9900991B, G0800235] Funding Source: researchfish
- Medical Research Council [G0800235] Funding Source: Medline
- Wellcome Trust Funding Source: Medline
Cortisone, a glucocorticoid hormone, was first used to treat rheumatoid arthritis in humans in the late 1940s, for which Hench, Reichstein and Kendall were awarded a Nobel Prize in 1950 and which led to the discovery of the anti-inflammatory effects of glucocorticoids. To be effective, the intrinsically inert cortisone must be converted to the active glucocorticoid, cortisol, by the intracellular action of 11 P-hydroxysteroid dehydrogenase type 1 (11 beta-HSD1). Whilst orally administered cortisone is rapidly converted to the active hormone, cortisol, by first pass metabolism in the liver, recent work has highlighted an anti-inflammatory role for 11 beta-HSD1 within specific tissues, including in leukocytes. Here, we review recent evidence pertaining to the anti-inflammatory role of 11 beta-HSD1 and describe how inhibition of 11 beta-HSD1, as widely proposed for treatment of metabolic disease, may impact upon inflammation. Finally, the mechanisms that regulate 11 beta-HSD1 transcription will be discussed. (c) 2008 Elsevier Ireland Ltd. All rights reserved.
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