Protective effect of sesquiterpene lactone parthenolide on LPS-induced acute lung injury

Acute lung injury (ALI) is a respiratory failure disease and the major source of mortality in the critically ill patients. The main pathological changes involved in ALI include the excessive recruitment and activation of neutrophils by increased pro-inflammatory mediators. However, any specific ther...

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Bibliographic Details
Published in:Archives of pharmacal research 2016, 39(12), , pp.1716-1725
Main Authors: Jang, You Jin, Back, Moon Jung, Fu, Zhicheng, Lee, Joo Hyun, Won, Jong Hoon, Ha, Hae Chan, Lee, Hae Kyung, Jang, Ji Min, Choi, Jong Min, Kim, Dae Kyong
Format: Article
Language:English
Subjects:
A549 Cells
Acute Lung Injury - chemically induced
Acute Lung Injury - pathology
Acute Lung Injury - prevention & control
Animals
Anti-Inflammatory Agents, Non-Steroidal - pharmacology
Anti-Inflammatory Agents, Non-Steroidal - therapeutic use
Cell Survival - drug effects
Cell Survival - physiology
Humans
Lactones - pharmacology
Lactones - therapeutic use
Lipopolysaccharides - toxicity
Male
Medicine
Mice
Mice, Inbred C57BL
Pharmacology/Toxicology
Pharmacy
Protective Agents - pharmacology
Protective Agents - therapeutic use
Research Article
Sesquiterpenes - pharmacology
Sesquiterpenes - therapeutic use
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Summary:Acute lung injury (ALI) is a respiratory failure disease and the major source of mortality in the critically ill patients. The main pathological changes involved in ALI include the excessive recruitment and activation of neutrophils by increased pro-inflammatory mediators. However, any specific therapy for ALI has not been developed. The objective of this study was to investigate protective effects of parthenolide, a sesquiterpene lactone produced in feverfew, on LPS-induced lung injury. In the present study, parthenolide treatment reduced infiltration of inflammatory cells, airway permeability and production of pro-inflammatory cytokines in LPS-induced ALI mouse model. Further, LPS-stimulated phosphorylation of NF-κB, the key regulatory transcription factor in ALI, was inhibited by parthenolide treatment in lung epithelial BEAS-2B cells and alveolar macrophage MH-S cells. These results suggest that parthenolide may provide a beneficial therapeutic strategy for ALI.
ISSN:0253-6269
1976-3786
DOI:10.1007/s12272-016-0716-x