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Ulinastatin protects rats from sepsis‐induced acute lung injury by suppressing the JAK‐STAT3 pathway
Author(s) -
Wu Jian,
Yan Xin,
Jin Guoqiang
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.27550
Subject(s) - ulinastatin , sepsis , medicine , lung , tumor necrosis factor alpha , inflammation , pharmacology , immunology , anesthesia
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.