J Immunol 2001 Dec 15;167(12):7094-7101
Du C, Khalil MW, Sriram S.
Department of Neurology, Multiple Sclerosis Research Center, Vanderbilt University Medical Center, Nashville, TN 37212. Lawson Research Institute, St. Josephs Care Center, and Department of Medicine, Pharmacology, and Toxicology, University of Western Ontario, London, Ontario, Canada.
Experimental allergic encephalomyelitis (EAE) is a Th1-mediated inflammatory demyelinating disease in the CNS, an animal model of multiple sclerosis.
We have examined the effect of dehydroepiandrosterone (DHEA) on the development of EAE in mice.
The addition of DHEA to cultures of myelin basic protein-primed splenocytes resulted in a significant decrease in T cell proliferation and secretion of (pro)inflammatory cytokines (IFN-gamma, IL-12 p40, and TNF-alpha) and NO in response to myelin basic protein.
These effects were associated with a decrease in activation and translocation of NF-kappaB.
In vivo administration of DHEA significantly reduced the severity and incidence of acute EAE, along with a decrease in demyelination/inflammation and expressions of (pro)inflammatory cytokines in the CNS.
These studies suggest that DHEA has
potent anti-inflammatory properties, which at least are in part mediated
by its inhibition of NF-kappaB activation.
PMID: 11739531 [PubMed - as supplied
PMID: 11739531 [PubMed - as supplied by publisher]