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乌司他丁通过抑制JAK-STAT3信号通路保护大鼠免受脓毒症诱导的急性肺损伤。

Ulinastatin protects rats from sepsis-induced acute lung injury by suppressing the JAK-STAT3 pathway.

作者信息

Wu Jian, Yan Xin, Jin Guoqiang

机构信息

Department of Pediatrics, The First Affiliated Hospital of Nanchang University, Nanchang, China.

Department of Health, The First Affiliated Hospital of Nanchang University, Nanchang, China.

出版信息

J Cell Biochem. 2019 Feb;120(2):2554-2559. doi: 10.1002/jcb.27550. Epub 2018 Sep 22.

DOI:10.1002/jcb.27550
PMID:30242880
Abstract

Sepsis is usually accompanied by pulmonary inflammations, leading to acute lung injury. During this process, endogenous factors that play a regulatory role could be exploited to therapeutically alleviate such lethal tissue injury. Here, we showed that ulinastatin (UTI) administration could reduce lung tissue necrosis and swelling during sepsis in rats. UTI treatment also decreased the levels of inflammatory mediators both in the lung and in the serum. Mechanistically, we showed that the phosphorylation levels of JAK2 and STAT3 in the lung of UTI-treated rats were lower than control rats and were correlated with the decreased levels of inflammatory mediators. Taken together, these results demonstrate the protective role of UTI in sepsis-induced acute lung injury.

摘要

脓毒症通常伴有肺部炎症,导致急性肺损伤。在此过程中,可以利用起调节作用的内源性因子来治疗性减轻这种致命的组织损伤。在这里,我们表明给予乌司他丁(UTI)可减少大鼠脓毒症期间的肺组织坏死和肿胀。UTI治疗还降低了肺组织和血清中炎症介质的水平。从机制上讲,我们表明UTI治疗的大鼠肺中JAK2和STAT3的磷酸化水平低于对照大鼠,并且与炎症介质水平的降低相关。综上所述,这些结果证明了UTI在脓毒症诱导的急性肺损伤中的保护作用。

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