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首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >Low susceptibility of NC/Nga mice to tumor necrosis factor-alpha-mediated lethality and hepatocellular damage with D-galactosamine sensitization.
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Low susceptibility of NC/Nga mice to tumor necrosis factor-alpha-mediated lethality and hepatocellular damage with D-galactosamine sensitization.

机译：NC / Nga小鼠对肿瘤坏死因子-α介导的致死性和D-半乳糖胺致肝细胞损伤的敏感性较低。

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摘要

The susceptibility of NC/Nga mice to tumor necrosis factor (TNF)-alpha was examined by using sensitization with d-galactosamine (d-GalN). Administration of TNF-alpha and d-GalN killed none of the NC/Nga mice, whereas it killed all of the BALB/c mice. Treatment with TNF-alpha and d-GalN caused few hepatic lesions in NC/Nga mice but massive hepatocellular apoptosis in BALB/c mice. Unlike BALB/c mice, there was no elevation in caspase 3 and 8 activities in the livers of NC/Nga mice receiving TNF-alpha and d-GalN. On the other hand, administration of anti-Fas antibody definitely killed both NC/Nga and BALB/c mice via activation of caspases 3 and 8. Treatment with TNF-alpha and d-GalN led to translocation of nuclear factor (NF)-kappaB in NC/Nga and BALB/c mice. However, NF-kappaB translocation was sustained in NC/Nga mice, although it disappeared in BALB/c mice 7 h after the treatment. NF-kappaB inhibitors activated caspases 3 and 8, and enhanced TNF-alpha-mediated lethality in NC/Nga. Taken together, the low susceptibility of NC/Nga mice to TNF-alpha-mediated lethality was suggested to be responsible for the sustained NF-kappaB activation.
机译：通过使用d-半乳糖胺（d-GalN）敏化检测了NC / Nga小鼠对肿瘤坏死因子（TNF）-α的敏感性。给予TNF-α和d-GalN不会杀死任何NC / Nga小鼠，而杀死所有的BALB / c小鼠。 TNF-α和d-GalN的治疗在NC / Nga小鼠中几乎没有引起肝脏损伤，但在BALB / c小鼠中却引起大量肝细胞凋亡。与BALB / c小鼠不同，接受TNF-α和d-GalN的NC / Nga小鼠肝脏中caspase 3和8活性没有升高。另一方面，抗Fas抗体的给药肯定通过激活胱天蛋白酶3和8杀死了NC / Nga和BALB / c小鼠。TNF-α和d-GalN的处理导致核因子（NF）-κB的移位在NC / Nga和BALB / c小鼠中。然而，尽管在处理后7小时BALF / c小鼠中NF-kappaB易位消失，但NC / Nga小鼠中NF-kappaB易位。 NF-κB抑制剂可激活胱天蛋白酶3和8，并增强TNF-α介导的NC / Nga杀伤力。两者合计，NC / Nga小鼠对TNF-α介导的致死性的低敏感性被认为是持续的NF-κB活化的原因。

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