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内毒素对大鼠肺氧中毒的保护作用:细胞因子可能参与其中。

Endotoxin protection of rats from pulmonary oxygen toxicity: possible cytokine involvement.

作者信息

Berg J T, Allison R C, Prasad V R, Taylor A E

机构信息

Department of Physiology, College of Medicine, University of South Alabama, Mobile 36688.

出版信息

J Appl Physiol (1985). 1990 Feb;68(2):549-53. doi: 10.1152/jappl.1990.68.2.549.

Abstract

Treatment with endotoxin protects rats against lung injury during hyperoxia (greater than 98% oxygen at 1 atmosphere absolute for 60 h). This study demonstrates that serum from endotoxin-treated donor rats also protects recipients from oxygen toxicity. Rats treated with serum from saline-treated donors were not protected, and protection was not explained by residual endotoxin in protective sera. Unlike endotoxin-protected rats (where lung antioxidant enzyme activity is elevated after hyperoxia), postexposure superoxide dismutase (SOD) and catalase (CAT) activities in the lungs of serum-protected rats were not affected. Levels of tumor necrosis factor (TNF) and interleukin 1 (IL-1) in protective sera were increased. This study demonstrates that increases in lung SOD and CAT activity are not required for endotoxin protection from hyperoxia and suggests that TNF and IL-1 may participate in the mechanism of endotoxin protection.

摘要

内毒素治疗可保护大鼠免受高氧(在1个绝对大气压下氧气浓度大于98%,持续60小时)期间的肺损伤。本研究表明,来自经内毒素治疗的供体大鼠的血清也可保护受体免受氧中毒。用来自经生理盐水治疗的供体的血清处理的大鼠未得到保护,保护性血清中的残余内毒素也无法解释这种保护作用。与经内毒素保护的大鼠(高氧后肺抗氧化酶活性升高)不同,血清保护的大鼠肺中暴露后的超氧化物歧化酶(SOD)和过氧化氢酶(CAT)活性未受影响。保护性血清中肿瘤坏死因子(TNF)和白细胞介素1(IL-1)的水平升高。本研究表明,内毒素保护大鼠免受高氧损伤并不需要肺SOD和CAT活性增加,并提示TNF和IL-1可能参与内毒素保护机制。

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