Sugama Shuei, Takenouchi Takato, Kitani Hiroshi, Fujita Masayo, Hashimoto Makoto
Department of Physiology, Nippon Medical School, 1-1-5 Sendagi Bunkyo-ku, Tokyo 113-8526, Japan.
J Neuroimmunol. 2007 Dec;192(1-2):31-9. doi: 10.1016/j.jneuroim.2007.08.016. Epub 2007 Oct 31.
The main objective of the present study was to determine if activin might inhibit microglial activation. In murine MG6 microglial cell cultures, lipopolysaccharide (LPS)-induced activation of these cells was mitigated by pretreatment with activin as assessed by compromised up-regulation of proinflammatory markers, including IL-18, IL-6 and iNOS. The suppressive effects of activin on microglial activation were similarly observed in rat brains administered with LPS into the lateral ventricle. The expression of activin mRNA was induced by treatment with LPS in both cell cultures and brains. Thus, activin might act as an anti-inflammatory cytokine produced by microglia, presumably modulating inflammation through an autocrine fashion.
本研究的主要目的是确定激活素是否可能抑制小胶质细胞的活化。在鼠MG6小胶质细胞培养物中，通过促炎标志物（包括IL-18、IL-6和诱导型一氧化氮合酶）上调减弱的情况评估，激活素预处理减轻了脂多糖（LPS）诱导的这些细胞的活化。在向侧脑室内注射LPS的大鼠脑中同样观察到激活素对小胶质细胞活化的抑制作用。在细胞培养物和脑中，LPS处理均可诱导激活素mRNA的表达。因此，激活素可能作为小胶质细胞产生的一种抗炎细胞因子，大概通过自分泌方式调节炎症。
