Administration of dehydroepiandrosterone ameliorates experimental autoimmune neuritis in Lewis rats
Autor: | Chang-Wen Shi, Xiao-dong Tan, Ruo-Peng Sun, Rui-Sheng Duan, Ying-Chun Dou |
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Rok vydání: | 2009 |
Předmět: |
medicine.medical_specialty
T-Lymphocytes medicine.medical_treatment T cell Freund's Adjuvant Immunology Neuritis Dehydroepiandrosterone Enzyme-Linked Immunosorbent Assay Spleen Lymphocyte proliferation Interferon-gamma Adjuvants Immunologic Peripheral Nervous System Neoplasms Internal medicine Lewis rats Animals Immunology and Allergy Medicine Myelin Sheath Cell Proliferation Analysis of Variance Dose-Response Relationship Drug business.industry Interferon-alpha Inflammatory cell infiltration Neuritis Autoimmune Experimental Rats Disease Models Animal Endocrinology medicine.anatomical_structure Cytokine Neurology Rats Inbred Lew Cattle Female Neurology (clinical) business |
Zdroj: | Journal of Neuroimmunology. 207:39-44 |
ISSN: | 0165-5728 |
DOI: | 10.1016/j.jneuroim.2008.11.011 |
Popis: | Dehydroepiandrosterone (DHEA) is an abundant adrenal steroid in serum of humans, and has been reported to have anti-inflammatory, anti-proliferative, and certain immune-regulating properties. Experimental autoimmune neuritis (EAN) is a Th1 cell-mediated animal model of Guillain-Barré syndrome (GBS) in humans. In the present study, DHEA was administered subcutaneously to Lewis rats immunized with bovine peripheral myelin (BPM) in Freund's complete adjuvant. Rats treated with DHEA displayed significant delay in onset, decreased inflammatory cell infiltration in the PNS. Benefit was associated with significant decreases in numbers of IFN-gamma and TNF-alpha expressing cells in the PNS, BPM-stimulated T cell proliferation and IFN-gamma, TNF-alpha-secretion in the spleen cells. Only 2 mg DHEA-treated EAN rats decreased peak clinical score. No significant difference of supernatant IL-10 was found among the treatment and control groups. These results suggest that DHEA can ameliorate the severity of EAN by suppressing the proliferation of autoreactive T cell and expression of pro-inflammatory cytokines. |
Databáze: | OpenAIRE |
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