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新生儿细胞免疫系统不成熟 ,患内毒素血症后易发展成为粒细胞减少症 ,其机制可能与活性氧 (ROS)和肿瘤坏死因子等多种炎性介质参与 ,引起粒细胞生成减少和 或粒细胞破坏增多有关。ROS不但可介导炎性损伤 ,而且作为一种具有高度活性和非特异的分子 ,可以调控细胞增殖和凋亡过程。新生儿产生ROS等炎性介质的水平与成人亦有不同。抗氧化剂如N 乙酰半胱氨酸可清除ROS ,阻断细胞内核因子 κB的活性 ,减少细胞因子的产生 ,有利于减少脂多糖引起的氧化抑制和相关脂质过氧化产物的形成 ,调节细胞的增殖和凋亡。
Neonatal cellular immune system immature, prone to endocytosis after the development of neutropenia, its mechanism may be reactive oxygen species (ROS) and tumor necrosis factor and other inflammatory mediators involved, resulting in reduced neutrophil and or Increased damage to granulocytes. ROS not only mediates inflammatory injury, but also regulates cell proliferation and apoptosis as a highly active and nonspecific molecule. Newborns produce ROS and other inflammatory mediators and adults are also different levels. Antioxidants such as N-acetylcysteine can scavenge ROS, block the activity of nuclear factor kappa B, decrease the production of cytokines, decrease the inhibition of lipopolysaccharide-induced oxidation and the formation of related lipid peroxidation products, Proliferation and Apoptosis.