Granisetron protects polymicrobial sepsis-induced acute lung injury in mice
Autor: | Fangzhao Wang, Tanwei Gu, Shenhai Gong, Jun Wang, Aihua Liu, Guoquan Wei, Mengwei Niu, Zhanke He, Yong Jiang, Peng Chen |
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Rok vydání: | 2019 |
Předmět: |
Male
0301 basic medicine Lipopolysaccharide Inflammasomes MAP Kinase Signaling System THP-1 Cells Chemokine CXCL1 animal diseases medicine.medical_treatment Acute Lung Injury Chemokine CXCL2 Biophysics Lung injury Pharmacology Granisetron p38 Mitogen-Activated Protein Kinases Biochemistry Sepsis 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine NLR Family Pyrin Domain-Containing 3 Protein medicine Animals Humans Phosphorylation Lung Molecular Biology Chemotherapy business.industry Inflammasome Cell Biology respiratory system medicine.disease respiratory tract diseases Mice Inbred C57BL CXCL1 030104 developmental biology medicine.anatomical_structure Neutrophil Infiltration chemistry 030220 oncology & carcinogenesis Reactive Oxygen Species business medicine.drug |
Zdroj: | Biochemical and Biophysical Research Communications. 508:1004-1010 |
ISSN: | 0006-291X |
DOI: | 10.1016/j.bbrc.2018.12.031 |
Popis: | Sepsis is a serious condition with a high mortality rate worldwide. Granisetron is an anti-nausea drug for patients undergoing chemotherapy. Here we aimed to identify the novel effect of granisetron on sepsis-induced acute lung injury (ALI). Our results showed that mice treated with granisetron displayed less severe lung damage than controls. Granisetron administration reduced pulmonary neutrophil recruitment after CLP. Moreover, the expressions of Cxcl1 and Cxcl2 were diminished in the presence of granisetron in THP-1 macrophages after lipopolysaccharide exposure. Additionally, granisetron could inhibit the activation of p38 MAPK and NLRP3 inflammasome both in vivo and in vitro. Collectively, granisetron protects against sepsis-induced ALI by suppressing macrophage Cxcl1/Cxcl2 expression and neutrophil recruitment in the lung. |
Databáze: | OpenAIRE |
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