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Dehydroepiandrosterone selectively inhibits production of tumor necrosis factor α and Interlukin‐6 in astrocytes
Author(s) -
KipperGalperin Marianne,
Galilly Ruth,
Danenberg Haim D.,
Brenner Talma
Publication year - 1999
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/s0736-5748(99)00067-2
Subject(s) - dehydroepiandrosterone , neuroactive steroid , tumor necrosis factor alpha , nitric oxide , endocrinology , medicine , experimental autoimmune encephalomyelitis , in vivo , prostaglandin e , interleukin , immunology , interleukin 6 , prostaglandin e2 , encephalomyelitis , inflammation , central nervous system , biology , cytokine , androgen , receptor , hormone , microbiology and biotechnology , gabaa receptor
Dehydroepiandrosterone (DHEA) is a native neurosteroid with immunomodulating activity. DHEA effectively protects animals from several viral, bacterial and parasitic infections and it was suggested that its age‐associated decline is related with immunosenescence. In the present study we examined the ability of DHEA to inhibit the production of inflammatory mediators by mycoplasma‐stimulated glial cells and to change the course of acute central nervous system (CNS) inflammatory disease in vivo . Addition of DHEA (10 μ g/ml) markedly inhibited tumor necrosis factor α (TNF α ) and interlukin‐6 (IL‐6) production (98 and 95%, respectively), whereas nitric oxide (NO) and prostaglandin E 2 (PGE 2 ) production was not affected. However, daily administration of 0.5 mg DHEA to mice or 5 mg to rats did not change the clinical outcome of experimental autoimmune encephalomyelitis (EAE).