The value of the lipopolysaccharide-induced acute lung injury model in respiratory medicine

2010 ◽  
Vol 4 (6) ◽  
pp. 773-783 ◽  
Author(s):  
Hong Chen ◽  
Chunxue Bai ◽  
Xiangdong Wang
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Respiratory Medicine ◽  
Injury Model ◽  
Lung Injury Model

PULMONARY FIBROBLAST FUNCTION IN AN ACUTE LUNG INJURY MODEL

1994 ◽  
Vol 37 (1) ◽  
pp. 156
Author(s):  
Andrew Mikulaschek ◽  
Stantey Z Trooskin ◽  
Allen Nonn ◽  
Jason Winfield
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Injury Model ◽  
Lung Injury Model ◽  
Pulmonary Fibroblast

Derivation of recruitment function from the pressure–volume curve in an acute lung injury model

2015 ◽  
Vol 205 ◽  
pp. 16-20 ◽  
Author(s):  
Yoshihiro Uzawa ◽  
Mikiya Otsuji ◽  
Koichi Nakazawa ◽  
Wei Fan ◽  
Yoshitsugu Yamada
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Volume Curve ◽  
Pressure Volume Curve ◽  
Injury Model ◽  
Lung Injury Model

AIRWAY PRESSURE RELEASE VENTILATION (APRV) IN A PEDIATRIC ACUTE LUNG INJURY MODEL

1990 ◽  
Vol 18 (Supplement) ◽  
pp. S231 ◽  
Author(s):  
Lynn D. Martin ◽  
Anthony L. Bilenki ◽  
James F. Rafferty ◽  
Randall C. Wetzel
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Airway Pressure ◽  
Airway Pressure Release Ventilation ◽  
Pressure Release ◽  
Injury Model ◽  
Lung Injury Model ◽  
Pressure Release Ventilation

scholarly journals Effects of nebulized antithrombin and heparin on inflammatory and coagulation alterations in an acute lung injury model in rats

2019 ◽  
Vol 18 (3) ◽  
pp. 571-583 ◽  
Author(s):  
Marta Camprubí‐Rimblas ◽  
Neus Tantinyà ◽  
Raquel Guillamat‐Prats ◽  
Josep Bringué ◽  
Ferranda Puig ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Injury Model ◽  
Lung Injury Model

scholarly journals Levonadifloxacin, a Novel Benzoquinolizine Fluoroquinolone, Modulates Lipopolysaccharide-Induced Inflammatory Responses in Human Whole-Blood Assay and Murine Acute Lung Injury Model

2020 ◽  
Vol 64 (5) ◽  
Author(s):  
Anasuya Patel ◽  
Ganesh V. Sangle ◽  
Jinal Trivedi ◽  
Sushant A. Shengule ◽  
Deepak Thorve ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Whole Blood ◽  
Inflammatory Responses ◽  
Immunomodulatory Activity ◽  
Human Whole Blood ◽  
Injury Model ◽  
Cytokine Levels ◽  
Lung Injury Model ◽  
Clinical Benefits

ABSTRACT Fluoroquinolones are reported to possess immunomodulatory activity; hence, a novel benzoquinolizine fluoroquinolone, levonadifloxacin, was evaluated in lipopolysaccharide-stimulated human whole-blood (HWB) and mouse acute lung injury (ALI) models. Levonadifloxacin significantly mitigated the inflammatory responses in an HWB assay through inhibition of proinflammatory cytokines and in the ALI model by lowering lung total white blood cell count, myeloperoxidase, and cytokine levels. The immunomodulatory effect of levonadifloxacin, along with promising antibacterial activity, is expected to provide clinical benefits in the treatment of infections.

scholarly journals Attenuation of LPS-induced acute lung injury by continentalic acid in rodents through inhibition of inflammatory mediators correlates with increased Nrf2 protein expression

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Hassan Ali ◽  
Ashrafullah Khan ◽  
Jawad Ali ◽  
Hadayat Ullah ◽  
Adnan Khan ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Treated Group ◽  
Protein Targets ◽  
Stress Markers ◽  
Injury Model ◽  
Tnf Α ◽  
Lung Injury Model ◽  
Continentalic Acid ◽  
Nrf2 Protein

Abstract Background Acute lung injury (ALI) together with acute respiratory distress syndrome (ARDS) are associated with high rate of mortality and morbidity in patients. In the current study, the anti-inflammatory effects of continentalic acid (CNT) in LPS-induced acute lung injury model was explored. Methods The acute lung injury model was established by administering LPS (5 mg/kg) intraperitonealy. Following LPS administration, the survival rate, temperature changes and lung Wet/Dry ratio were assessed. The antioxidants (GSH, GST, Catalase and SOD) and oxidative stress markers (MDA, NO, MPO) were evaluated in all the treated groups. Similarly, the cytokines such as IL-1β, IL-6 and TNF-α were analyzed using ELISA assay. The histological changes were determined using H and E staining, while Nrf2 and iNOS level were determined using immunohistochemistry analysis. The molecular docking analysis was performed to assess the pharmacokinetics parameters and interaction of the CNT with various protein targets. Results The results showed that CNT dose dependently (10, 50 and 100 mg/kg) reduced mortality rate, body temperature and lungs Wet/Dry ratio. CNT post-treatment significantly inhibited LPS-induced production of pro-inflammatory cytokines such as IL-1β, IL-6 and TNF-α. The CNT post-treatment markedly improved the hematological parameters, while significantly reduced the MPO (indicator of the neutrophilic infiltration) activity compared to the LPS treated group. Furthermore, the CNT (100 mg/kg) post-administration remarkably inhibited the lung Wet/Dry ratio. The CNT (100 mg/kg) treated group showed marked reduction in the oxidative stress markers such as malonaldehyde (MDA) and Nitric oxide (NO) concentration, while induced the level of the anti-oxidant enzymes such as GST, GSH, Catalase and SOD. Similarly, the CNT markedly reduced the iNOS expression level, while induced the Nrf2 protein expression. Additionally, the molecular docking study showed significant binding interaction with the Nrf2, p65, Keap1, HO-1, IL-1β, IL-6, TNF-α and COX-2, while exhibited excellent physicochemical properties. Conclusion The CNT showed marked protection against the LPS-induced lung injury and improved the behavioral, biochemical and histological parameters. Furthermore, the CNT showed significant interaction with several protein targets and exhibited better physicochemical properties.

Sign in / Sign up

Export Citation Format

Share Document