Administration of dehydroepiandrosterone suppresses experimental allergic encephalomyelitis in SJL/J mice
Administration of dehydroepiandrosterone suppresses experimental allergic encephalomyelitis in SJL/J mice
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DOI：
10.4049/jimmunol.167.12.7094
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发表时间：
2001-12-15
影响因子：
4.4
通讯作者：
Sriram, S
中科院分区：
文献类型：
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作者：
Du, CG;Khalil, MW;Sriram, S
实验性变态反应性脑脊髓炎（EAE）是一种Th 1介导的中枢神经系统炎性脱髓鞘疾病，是多发性硬化症的动物模型。我们研究了脱氢表雄酮（DHEA）对小鼠EAE发展的影响。将DHEA添加到髓磷脂碱性蛋白致敏的脾细胞的培养物中导致响应于髓磷脂碱性蛋白的T细胞增殖和（促）炎性细胞因子（IFN-γ、IL-12 p40和TNF-α）和NO的分泌显著降低。这些作用与NF-κ B的活化和易位减少有关。DHEA的体内给药显著降低了急性EAE的严重程度和发生率，沿着CNS中脱髓鞘/炎症和（促）炎性细胞因子表达的减少。这些研究表明，DHEA具有有效的抗炎特性，这至少部分是由其抑制NF-κ B活化介导的。
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.