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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.
|Number of pages||9|
|Journal||Molecular and Cellular Endocrinology|
|Publication status||Published - 25 Mar 2009|
- 11β-Hydroxysteroid dehydrogenase
- Mast cell
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- 1 Finished
How does 11B-hydroxysteriod dehydrogenase type 1 limit inflammation.
Chapman, K., Gray, M., Savill, J. & Seckl, J.
1/10/08 → 30/04/12