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首页> 外文期刊>Journal of Cellular Physiology >Possible involvement of reactive oxygen species in D-galactosamine-induced sensitization against tumor necrosis factor-alpha-induced hepatocyte apoptosis.
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Possible involvement of reactive oxygen species in D-galactosamine-induced sensitization against tumor necrosis factor-alpha-induced hepatocyte apoptosis.

机译：可能的活性氧参与D-galactosamine-induced敏化对肿瘤坏死factor-alpha-induced肝细胞细胞凋亡。

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摘要

Intravenous administration of tumor necrosis factor-alpha (TNF-alpha) (0.5 microg/mouse) caused hepatocyte apoptosis in BALB/c mice when they were sensitized with D-galactosamine (GalN, 20 mg/mouse). Activation of nuclear factor kappa B (NF-kappa B) and expression of apoptotic Bcl-2 family members were not significantly different between livers of mice treated with TNF-alpha alone and GalN + TNF-alpha, indicating that neither activation of NF-kappa B nor expression of Bcl-2 family is involved in the sensitization by GalN against TNF-alpha-induced hepatocyte apoptosis. To identify differentially expressed genes implicated in GalN-induced hepatocyte sensitization, we adopted mRNA fingerprinting using an arbitrarily primed polymerase chain reaction. The present analysis revealed that mRNA expression of extracellular antioxidant, selenoprotein P, was up-regulated in the livers after GalN administration. GalN-induced increase in its protein level was confirmed by Western blotting. Increased expression of this gene was also observed in the liver of mice treated with concanavalin A, but not anti-Fas antibody. mRNA of another antioxidant, glutathione peroxidase-1, was also up-regulated, and lipid peroxides were produced in the liver after GalN administration. Selenoprotein P mRNA level also increased in Huh-7 human hepatoma cells incubated with GalN (5 or 10 mM). Accordingly, formation of reactive oxygen species (ROS) was observed in GalN-treated Huh-7 cells. H(2)O(2) induced up-regulation of selenoprotein P mRNA and sensitized Huh-7 cells to TNF-alpha-induced apoptosis. These results suggest that ROS produced by GalN may play a pivotal role in hepatocyte sensitization toward TNF-alpha-induced apoptosis. Copyright 2001 Wiley-Liss, Inc.
机译：静脉注射肿瘤坏死因子-α(tnf) (0.5 microg /鼠标)在BALB / c小鼠肝细胞凋亡引起的他们敏感D-galactosamine (GalN20毫克/鼠标)。B (nf -κB)和bcl - 2表达凋亡家庭成员没有显著不同之间与tnf治疗组小鼠的肝脏单独和GalN + tnf,表明激活nf -κB和表达式bcl - 2家族参与了敏化通过对TNF-alpha-induced GalN肝细胞细胞凋亡。基因涉及GalN-induced肝细胞敏化作用,我们采用mRNA指纹使用任意聚合酶链式的反应。表达的细胞外抗氧化剂,硒蛋白P,上调了肝脏后GalN管理。在证实了西方的蛋白质水平印迹。也观察到治疗组小鼠的肝脏伴刀豆球蛋白A,但不是anti-Fas抗体。新发现的抗氧化剂,谷胱甘肽peroxidase-1也上调,脂质过氧化物是什么生产后的肝脏GalN管理。硒蛋白P mRNA水平也在增加与GalN Huh-7人类肝癌细胞孵化(5或者10毫米)。在GalN-treated氧物种(ROS)观察Huh-7细胞。硒蛋白P mRNA和敏化Huh-7细胞TNF-alpha-induced细胞凋亡。建议GalN会产生的活性氧在肝细胞致敏向关键的作用TNF-alpha-induced细胞凋亡。Wiley-Liss公司。

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