The unique molecular targets associated antioxidant and antifibrotic activity of curcumin in in vitro model of acute lung injury: A proteomic approach

BioFactors ◽  
2021 ◽  
Author(s):  
Sadiya Bi Shaikh ◽  
Mohd Altaf Najar ◽  
Ashwini Prabhu ◽  
D. A. B. Rex ◽  
Jaikanth Chanderasekaran ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
In Vitro Model ◽  
Molecular Targets ◽  
Proteomic Approach ◽  
Vitro Model

scholarly journals Adrenomedullin expression in a rat model of acute lung injury induced by hypoxia and LPS

2005 ◽  
Vol 288 (3) ◽  
pp. L536-L545 ◽  
Author(s):  
Jackeline Agorreta ◽  
Javier J. Zulueta ◽  
Luis M. Montuenga ◽  
Mercedes Garayoa
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Cell Lines ◽  
Rat Model ◽  
In Vitro Model ◽  
Rat Lung ◽  
Vitro Model

Adrenomedullin (ADM) is upregulated independently by hypoxia and LPS, two key factors in the pathogenesis of acute lung injury (ALI). This study evaluates the expression of ADM in ALI using experimental models combining both stimuli: an in vivo model of rats treated with LPS and acute normobaric hypoxia (9% O2) and an in vitro model of rat lung cell lines cultured with LPS and exposed to hypoxia (1% O2). ADM expression was analyzed by in situ hybridization, Northern blot, Western blot, and RIA analyses. In the rat lung, combination of hypoxia and LPS treatments overcomes ADM induction occurring after each treatment alone. With in situ techniques, the synergistic effect of both stimuli mainly correlates with ADM expression in inflammatory cells within blood vessels and, to a lesser extent, to cells in the lung parenchyma and bronchiolar epithelial cells. In the in vitro model, hypoxia and hypoxia + LPS treatments caused a similar strong induction of ADM expression and secretion in epithelial and endothelial cell lines. In alveolar macrophages, however, LPS-induced ADM expression and secretion were further increased by the concomitant exposure to hypoxia, thus paralleling the in vivo response. In conclusion, ADM expression is highly induced in a variety of key lung cell types in this rat model of ALI by combination of hypoxia and LPS, suggesting an essential role for this mediator in this syndrome.

scholarly journals Role of heparin in pulmonary cell populations in an in-vitro model of acute lung injury

2017 ◽  
Vol 18 (1) ◽  
Author(s):  
Marta Camprubí–Rimblas ◽  
Raquel Guillamat-Prats ◽  
Thomas Lebouvier ◽  
Josep Bringué ◽  
Laura Chimenti ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
In Vitro Model ◽  
Cell Populations ◽  
Vitro Model

MiR-494-3p alleviates acute lung injury through regulating NLRP3 activation by targeting CMPK2

2021 ◽  
pp. 1-10
Author(s):  
Hong Wang ◽  
Shuqin Wang ◽  
Shanshan Huang
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Inflammatory Response ◽  
Nlrp3 Inflammasome ◽  
Cell Apoptosis ◽  
In Vitro Model ◽  
In Vivo Model ◽  
Respiratory Disorder ◽  
Vitro Model

Acute lung injury (ALI) is a severe respiratory disorder with a high rate of mortality, and is characterized by excessive cell apoptosis and inflammation. MicroRNAs (miRNAs) play pivotal roles in ALI. This study examined the biological function of miR-494-3p in cell apoptosis and inflammatory response in ALI. For this, mice were injected with lipopolysaccharide (LPS) to generate an in-vivo model of ALI (ALI mice), and WI-38 cells were stimulated with lipopolysaccharide (LPS) to generate an in-vitro model of ALI. We found that miR-494-3p was significantly downregulated in the ALI mice and in the in-vitro model. Overexpression of miR-494-3p inhibited inflammation and cell apoptosis in the LPS-induced WI-38 cells, and improved the symptoms of lung injury in the ALI mice. We then identified cytidine/uridine monophosphate kinase 2 (CMPK2) as a novel target of miR-494-3p in the WI-38 cells. Furthermore, miR-494-3p suppressed cell apoptosis and the inflammatory response in LPS-treated WI-38 cells through targeting CMPK2. The NLRP3 inflammasome is reportedly responsible for the activation of inflammatory processes. In our study, CMPK2 was confirmed to activate the NLRP3 inflammasome in LPS-treated WI-38 cells. In conclusion, miR-494-3p attenuates ALI through inhibiting cell apoptosis and the inflammatory response by targeting CMPK2, which suggests the value of miR-494-3p as a target for the treatment for ALI.

scholarly journals An in Vitro Model of Blast Induce Lung Injury using Shock Tube

2019 ◽  
Vol 2 (2) ◽  
pp. 1-9
Author(s):  
Zhixin Liang ◽  
Zhaorui Zhang ◽  
Huaidong Li ◽  
Liang’an Chen
Keyword(s):  
Lung Injury ◽  
Shock Tube ◽  
In Vitro Model ◽  
Induce Lung Injury ◽  
Vitro Model

scholarly journals Role of LecA and LecB Lectins in Pseudomonas aeruginosa-Induced Lung Injury and Effect of Carbohydrate Ligands

2009 ◽  
Vol 77 (5) ◽  
pp. 2065-2075 ◽  
Author(s):  
Chanez Chemani ◽  
Anne Imberty ◽  
Sophie de Bentzmann ◽  
Maud Pierre ◽  
Michaela Wimmerová ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Parental Strain ◽  
A549 Cells ◽  
Carbohydrate Ligands ◽  
Vitro Model

ABSTRACT Pseudomonas aeruginosa is a frequently encountered pathogen that is involved in acute and chronic lung infections. Lectin-mediated bacterium-cell recognition and adhesion are critical steps in initiating P. aeruginosa pathogenesis. This study was designed to evaluate the contributions of LecA and LecB to the pathogenesis of P. aeruginosa-mediated acute lung injury. Using an in vitro model with A549 cells and an experimental in vivo murine model of acute lung injury, we compared the parental strain to lecA and lecB mutants. The effects of both LecA- and Lec B-specific lectin-inhibiting carbohydrates (α-methyl-galactoside and α-methyl-fucoside, respectively) were evaluated. In vitro, the parental strain was associated with increased cytotoxicity and adhesion on A549 cells compared to the lecA and lecB mutants. In vivo, the P. aeruginosa-induced increase in alveolar barrier permeability was reduced with both mutants. The bacterial burden and dissemination were decreased for both mutants compared with the parental strain. Coadministration of specific lectin inhibitors markedly reduced lung injury and mortality. Our results demonstrate that there is a relationship between lectins and the pathogenicity of P. aeruginosa. Inhibition of the lectins by specific carbohydrates may provide new therapeutic perspectives.

Critical evaluation of emergency stockpile ventilators in an in vitro model of pediatric lung injury

2011 ◽  
Vol 12 (6) ◽  
pp. e357-e361 ◽  
Author(s):  
Jason W. Custer ◽  
Christopher M. Watson ◽  
Joe Dwyer ◽  
David W. Kaczka ◽  
Brett A. Simon ◽  
...  
Keyword(s):  
Lung Injury ◽  
In Vitro Model ◽  
Critical Evaluation ◽  
Vitro Model

scholarly journals Impact of oxidative stress on epithelial repair and alveolar oedema, within in vitro model of lung injury

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Cécile Chupin ◽  
Anik Privé ◽  
Emmanuelle Brochiero ◽  
Yves Berthiaume
Keyword(s):  
Oxidative Stress ◽  
Lung Injury ◽  
In Vitro Model ◽  
Epithelial Repair ◽  
Vitro Model ◽  
Alveolar Oedema
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