Perinatal Center, Dept. of Physiology and Neuroscience and Dept of Paediatrics, Sahlgrenska Academy, University of Gothenburg, Sweden.
Neurobiol Dis. 2010 Apr;38(1):36-46. doi: 10.1016/j.nbd.2009.12.024. Epub 2010 Jan 4.
Inflammation induced by hypoxia-ischemia (HI) contributes to the development of injury in the newborn brain. In this study, we investigated the role of galectin-3, a novel inflammatory mediator, in the inflammatory response and development of brain injury in a mouse model for neonatal HI. Galectin-3 gene and protein expression was increased after injury and galectin-3 was located in activated microglia/macrophages. Galectin-3-deficient mice (gal3-/-) were protected from injury particularly in hippocampus and striatum. Microglia accumulation was increased in the gal3-/- mice but accompanied by decreased levels of total matrix metalloproteinase (MMP)-9 and nitrotyrosine. The protection and increase in microglial infiltration was more pronounced in male gal3-/- mice. Trophic factors and apoptotic markers did not significantly differ between groups. In conclusion, galectin-3 contributes to neonatal HI injury particularly in male mice. Our results indicate that galectin-3 exerts its effect by modulating the inflammatory response.
缺氧缺血（HI）引起的炎症反应导致新生儿脑损伤的发生。在这项研究中，我们研究了半乳糖凝集素-3（一种新型炎症介质）在新生 HI 小鼠模型中炎症反应和脑损伤发展中的作用。损伤后半乳糖凝集素-3基因和蛋白表达增加，半乳糖凝集素-3位于活化的小胶质细胞/巨噬细胞中。半乳糖凝集素-3 缺陷型（gal3-/-）小鼠对损伤具有保护作用，特别是在海马体和纹状体。gal3-/-小鼠中的小胶质细胞聚集增加，但总基质金属蛋白酶（MMP）-9 和硝基酪氨酸的水平降低。雄性 gal3-/-小鼠中的保护作用和小胶质细胞浸润增加更为明显。营养因子和凋亡标志物在各组之间无显著差异。总之，半乳糖凝集素-3导致新生 HI 损伤，特别是在雄性小鼠中。我们的结果表明，半乳糖凝集素-3通过调节炎症反应发挥作用。
