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首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >The cyclopentone prostaglandin 15-deoxy-Delta(12,14) prostaglandin J2 represses nitric oxide, TNF-alpha, and IL-12 production by microglial cells.
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The cyclopentone prostaglandin 15-deoxy-Delta(12,14) prostaglandin J2 represses nitric oxide, TNF-alpha, and IL-12 production by microglial cells.

机译：环戊酮前列腺素15-脱氧-Delta（12,14）前列腺素J2抑制小胶质细胞产生一氧化氮，TNF-α和IL-12。

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Prostaglandins are generally considered pro-inflammatory molecules that contribute to the pathology associated with a variety of immune-mediated diseases including multiple sclerosis. However, recently it has been demonstrated that specific cyclopentone prostaglandin metabolites including 15-deoxy-Delta(12,14) prostaglandin J2 (15d-PGJ2) are capable of repressing the production of pro-inflammatory molecules by cells of the monocyte/macrophage lineage. Activated microglia produce nitric oxide (NO) and TNF-alpha, molecules which can be toxic to cells including oligodendrocytes, thus potentially contributing to the pathology associated with multiple sclerosis. The current study demonstrates that 15d-PGJ2 inhibits lipopolysachharide (LPS) induction of NO and TNF-alpha production by rat primary microglia and mouse N9 microglial cells. 15d-PGJ2 also inhibits NO production by microglial cells activated in response to IFN-gamma and TNF-alpha, cytokines believed to be important modulators of multiple sclerosis. IL-12 plays a critical role in stimulating the production of Th1 cells, which are believed to contribute to the pathology associated with multiple sclerosis. The current studies demonstrate that 15d-PGJ2 represses the production of IL-12 by microglial cells. Collectively, these studies demonstrate that the prostaglandin metabolite 15d-PGJ2 represses microglial production of potentially cytotoxic molecules, as well as molecules capable of altering T-cell phenotype. These in vitro studies suggest the possibility that the prostaglandin 15d-PGJ2 may modulate inflammatory diseases including multiple sclerosis.
机译：前列腺素通常被认为是促炎分子，其促成与包括多发性硬化症在内的多种免疫介导疾病相关的病理。但是，最近已经证明，包括15-脱氧-Delta（12,14）前列腺素J2（15d-PGJ2）在内的特定环戊酮前列腺素代谢物能够抑制单核细胞/巨噬细胞谱系细胞产生促炎分子。活化的小胶质细胞产生一氧化氮（NO）和TNF-α分子，这些分子可能对包括少突胶质细胞在内的细胞有毒，因此可能导致与多发性硬化症相关的病理。当前的研究表明15d-PGJ2抑制大鼠原发小胶质细胞和小鼠N9小胶质细胞对脂多糖（LPS）诱导的NO和TNF-α的诱导。 15d-PGJ2还抑制由响应IFN-γ和TNF-α活化的小胶质细胞产生的NO，这些细胞因子被认为是多发性硬化症的重要调节剂。 IL-12在刺激Th1细胞产生中起关键作用，据信Th1细胞有助于与多发性硬化症相关的病理。目前的研究表明15d-PGJ2抑制小胶质细胞产生IL-12。这些研究共同表明，前列腺素代谢产物15d-PGJ2抑制潜在的细胞毒性分子以及能够改变T细胞表型的分子的小胶质细胞生成。这些体外研究表明，前列腺素15d-PGJ2可能调节包括多发性硬化症在内的炎症疾病。

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