...
首页> 外文期刊>The American journal of Chinese medicine >Effect of polysaccharide Krestin on the up-regulation of macrophage colony-stimulating factor gene expression in protecting mouse peritoneal macrophages from oxidative injury.
【24h】

Effect of polysaccharide Krestin on the up-regulation of macrophage colony-stimulating factor gene expression in protecting mouse peritoneal macrophages from oxidative injury.

机译:多糖Krestin对保护小鼠腹膜巨噬细胞免受氧化损伤的巨噬细胞集落刺激因子基因表达上调的影响。

获取原文
获取原文并翻译 | 示例
   

获取外文期刊封面封底 >>

       

摘要

Oxidative injury caused by oxidatively modified low density lipoprotein (Ox-LDL) plays an important role in the transformation of macrophages into foam cells and atherogenesis. Treatments to protect macrophages from oxidative injury will be effective in treating atherosclerosis. A macrophage-specific growth factor, macrophage colony-stimulating factor (M-CSF), was reported to be able to prevent the progression of atherosclerosis in Watanabe heritable hypercholesterolemic (WHHL) rabbits. A protein-bound polysaccharide, polysaccharide Krestin (PSK), was also proven to have effects in preventing atherosclerosis in our previous work. We proposed that, both M-CSF and PSK could protect macrophages from oxidative injury, and the effects of PSK were associated with its capability of inducing M-CSF expression. In our present results, M-CSF could alleviate the Ox-LDL- or tert-butyl hydroperoxide (tbOOH)-induced injury to mouse peritoneal macrophages, and PSK exhibited some similar effects. PSK treatment could induce M-CSF gene expression and secretion in mouse peritoneal macrophages. Furthermore actinomycin D and cycloheximide could attenuate that induction. We concluded that, maybe PSK exerted its effects on macrophages partly through the transcriptional induction of M-CSF in the cells.
机译:氧化修饰的低密度脂蛋白(Ox-LDL)引起的氧化损伤在巨噬细胞转化为泡沫细胞和动脉粥样硬化中起重要作用。保护巨噬细胞免受氧化损伤的治疗将有效治疗动脉粥样硬化。据报道,巨噬细胞特异性生长因子巨噬细胞集落刺激因子(M-CSF)能够预防渡边可遗传性高胆固醇血症(WHHL)兔的动脉粥样硬化进展。在我们以前的工作中,还证明了一种与蛋白质结合的多糖,即多糖Krestin(PSK)具有预防动脉粥样硬化的作用。我们提出,M-CSF和PSK均可保护巨噬细胞免受氧化损伤,并且PSK的作用与其诱导M-CSF表达的能力有关。在我们目前的结果中,M-CSF可以减轻Ox-LDL-或叔丁基氢过氧化物(tbOOH)引起的小鼠腹膜巨噬细胞损伤,而PSK表现出一些相似的作用。 PSK治疗可诱导小鼠腹膜巨噬细胞中M-CSF基因表达和分泌。此外,放线菌素D和环己酰亚胺可以减弱这种诱导作用。我们得出的结论是,也许PSK可能部分地通过细胞中M-CSF的转录诱导对巨噬细胞发挥作用。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号