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
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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