scholarly journals Role of insulin in oleic acid-induced acute lung injury in rat model

2021 ◽  
Vol 65 ◽  
pp. 103-108
Author(s):  
Sudhashekhar Kumar ◽  
Priyanka Bhagat ◽  
Shashikant C. U. Patne ◽  
Ratna Pandey
Keyword(s):  
Acute Lung Injury ◽  
Oleic Acid ◽  
Lung Injury ◽  
Water Content ◽  
Histological Examination ◽  
Rat Model ◽  
Control Group ◽  
Progressive Decrease ◽  
Immunomodulatory Agent ◽  
Group I

Objectives: Acute lung injury (ALI) is an inflammatory condition, therefore, this study was undertaken to determine the effect of insulin (an immunomodulatory agent) in oleic acid (OA)-induced ALI in rat model. Materials and Methods: The experiments were performed on adult male albino rats (total n = 18). The trachea, jugular vein and carotid artery of anaesthetised adult rats were cannulated to keep the respiratory tract patent, deliver saline/drugs and recording of blood pressure, respectively. Animals were divided into three groups. In Group I (control group), normal saline (75 μL) was injected and this group served as control group. In Group II (OA group), OA (75 μL) was administered to induce ALI in rats. In Group III (insulin + OA), OA (75 μL) was injected in insulin pre-treated rats. Respiratory frequency (RF), heart rate (HR) and mean arterial pressure (MAP) were recorded on computerised chart recorder; arterial blood sample was collected to determine PaO2/FiO2. Further, pulmonary water content was determined, and histological examination of the lung was done in all animals. Results: Injection of OA produced ALI indicated by significant increase in RF by 30 min followed by progressive decrease and ultimately death of animal. Significant increase in the pulmonary water content and decrease in PaO2/FiO2 were observed in these animals. Histological examination of lungs showed damage to the lung parenchyma. An immediate decrease in HR and MAP followed by some improvement and then progressive decrease was also observed. Conclusions: Insulin (an immunomodulatory agent) pre-treatment delayed initiation of OA-induced ALI as indicated by protection against OA-induced severe alteration in the RF in the initial stage and less lung injury in histological examination, although; it could not alter the overall course of the disease.

scholarly journals WITHDRAWN: The effect of coenzyme q10 on a rat model of oleic acid-induced acute lung injury

2013 ◽  
Author(s):  
Melike Korkmaz ◽  
I. Aydin Erden ◽  
Sennur Uzun ◽  
S. Banu Akinci ◽  
Gonul Erden ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Oleic Acid ◽  
Lung Injury ◽  
Rat Model ◽  
Coenzyme Q10

scholarly journals Keratinocyte Growth Factor-2 Reduces Inflammatory Response to Acute Lung Injury Induced by Oleic Acid in Rats by Regulating Key Proteins of the Wnt/β-Catenin Signaling Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Shao Tenghao ◽  
Chen Ning ◽  
Wang Shenghai ◽  
Sun Qinlong ◽  
Wu Jiaqian ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Oleic Acid ◽  
Lung Injury ◽  
Signaling Pathway ◽  
Lung Tissue ◽  
Blood Cells ◽  
Keratinocyte Growth Factor ◽  
White Blood Cells ◽  
Inflammatory Factors ◽  
Control Group

Reducing inflammation can effectively relieve acute lung injury (ALI). Objective. To test whether keratinocyte growth factor-2 (KGF-2) can reduce oleic acid-induced inflammation in ALI of rats and explore its possible mechanism. Methods. 45 Sprague-Dawley rats were randomly divided into control group, ALI group, and ALI + KGF-2 group. The animal model of acute lung injury was established by injecting 0.1 mL/kg oleic acid into the tail vein of rats. Rats in the control group were injected with equal volume of normal saline (NS). Each group needs pretreatment 72 hours before the preparation of the acute lung injury model. The control group and ALI group were instilled with 5 ml/kg NS through the airway, and the same amount of KGF-2 was instilled in the ALI + KGF-2 group. It takes 8 hours to successfully prepare the ALI model. Observe the pathological changes of lung tissue through light microscopy, ultrastructural changes through electron microscopy, and the lung wettability/dry weight (w/d) ratio and lung permeability index (LPI). By detecting changes in inflammatory factors in lung tissue and changes in the number of BALF cells, the changes in inflammation in each group were observed. The expressions of Wnt5a, β-catenin, and APC in lung tissue were detected by immunohistochemistry and Western blot. The changes of key proteins in Wnt/β-catenin signaling pathway in the lung tissue of each group were observed. Result. Compared with the ALI group, after KGF-2 pretreatment, the degree of lung injury was reduced, the expression of inflammatory factors was reduced, and the number of red blood cells and white blood cells in BALF was reduced. It can also be observed that the expression of Wnt5a, β-catenin, and APC, a key protein in the Wnt/β-catenin signaling pathway, is reduced. The analysis showed that the number of inflammatory factors, red blood cells, and white blood cells in BALF was positively correlated with the expression of Wnt5a, β-catenin, and APC. Conclusion. KGF-2 may reduce the inflammatory response in ALI induced by oleic acid by regulating key proteins in the Wnt/β-catenin signaling pathway.

Ulinastatin is a novel candidate drug for sepsis and secondary acute lung injury, evidence from an optimized CLP rat model

2013 ◽  
Vol 17 (3) ◽  
pp. 799-807 ◽  
Author(s):  
Ning Wang ◽  
Xin Liu ◽  
Xinchuan Zheng ◽  
Hongwei Cao ◽  
Guo Wei ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Rat Model ◽  
Candidate Drug

The differential expression of novel circular RNAs in an acute lung injury rat model caused by smoke inhalation

2017 ◽  
Vol 74 (1) ◽  
pp. 25-33 ◽  
Author(s):  
Zhiqiang Ye ◽  
Xuhui Liu ◽  
Yuewu Yang ◽  
Xianling Zhang ◽  
Ting Yu ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Differential Expression ◽  
Rat Model ◽  
Smoke Inhalation ◽  
Circular Rnas

scholarly journals Corrigendum to: Acute Lung Injury in A Rat Model Of Intestinal Ischemia-Reperfusion: The Potential Time Depended Role Of Phospholipases

2021 ◽  
Vol 263 ◽  
pp. 291
Author(s):  
Georgia Kostopanagiotou ◽  
Efthimios Avgerinos ◽  
Konstantinos Kostopanagiotou ◽  
Nikolaos Arkadopoulos ◽  
Ioanna Andreadou ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Rat Model ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion ◽  
Intestinal Ischemia Reperfusion

scholarly journals Effects of Antibiotic Therapy on Pseudomonas aeruginosa-Induced Lung Injury in a Rat Model

1999 ◽  
Vol 43 (10) ◽  
pp. 2389-2394 ◽  
Author(s):  
Erika J. Ernst ◽  
Satoru Hashimoto ◽  
Joseph Guglielmo ◽  
Teiji Sawa ◽  
Jean-Francois Pittet ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Rat Model ◽  
In Vivo Model ◽  
Antibiotic Administration ◽  
Lung Water ◽  
Alveolar Epithelial ◽  
The Right

ABSTRACT The effect of antibiotics on the acute lung injury induced by virulent Pseudomonas aeruginosa PA103 was quantitatively analyzed in a rat model. Lung injury was induced by the instillation of PA103 directly into the right lower lobes of the lungs of anesthetized rats. The alveolar epithelial injury, extravascular lung water, and total plasma equivalents were measured as separate, independent parameters of acute lung injury. Four hours after the instillation of PA103, all the parameters were increased linearly depending on the dose of P. aeruginosa. Next, we examined the effects of intravenously administered antibiotics on the parameters of acute lung injury in d-galactosamine-sensitized rats. One hour after the rats received 107 CFU of PA103, an intravenous bolus injection of aztreonam (60 mg/kg) or imipenem-cilastatin (30 mg/kg) was administered. Despite an MIC indicating resistance, imipenem-cilastatin improved all the measurements of lung injury; in contrast, aztreonam, which had an MIC indicating sensitivity, did not improve any of the lung injury parameters. The antibiotics did not generate different quantities of plasma endotoxin; therefore, endotoxin did not appear to explain the differences in lung injury. This in vivo model is useful to quantitatively compare the efficacies of parenteral antibiotic administration on Pseudomonas airspace infections.

Colloidal gold particles as a new in vivo marker of early acute lung injury

2004 ◽  
Vol 287 (4) ◽  
pp. L867-L878 ◽  
Author(s):  
Kai Heckel ◽  
Rainer Kiefmann ◽  
Martina Dörger ◽  
Mechthild Stoeckelhuber ◽  
Alwin E. Goetz
Keyword(s):  
Electron Microscopy ◽  
Acute Lung Injury ◽  
Gas Exchange ◽  
Lung Injury ◽  
Colloidal Gold ◽  
Microvascular Permeability ◽  
Arterial Oxygen ◽  
Control Group ◽  
Gold Particles

Permeability of the endothelial barrier to large molecules plays a pivotal role in the manifestation of early acute lung injury. We present a novel and sensitive technique that brings microanatomical visualization and quantification of microvascular permeability in line. White New Zealand rabbits were anesthetized and ventilated mechanically. Rabbit serum albumin (RSA) was labeled with colloidal gold particles. We quantified macromolecular leakage of gold-labeled RSA and thickening of the gas exchange distance by electron microscopy, taking into account morphology of microvessels. The control group receiving a saline solution represented a normal gas exchange barrier without extravasation of gold-labeled albumin. Infusion of lipopolysaccharide (LPS) resulted in a significant displacement of gold-labeled albumin into pulmonary cells, the lung interstitium, and even the alveolar space. Correspondingly, intravital fluorescence microscopy and digital image analysis indicated thickening of width of alveolar septa. The findings were accompanied by a deterioration of alveolo-arterial oxygen difference, whereas wet/dry ratio and albumin concentration in the bronchoalveolar lavage fluid failed to detect that early stage of pulmonary edema. Inhibition of the nuclear enzyme poly(ADP-ribose) synthetase by 3-aminobenzamide prevented LPS-induced microvascular injury. To summarize: colloidal gold particles visualized by standard electron microscopy are a new and very sensitive in vivo marker of microvascular permeability in early acute lung injury. This technique enabling detailed microanatomical and quantitative pathophysiological characterization of edema formation can form the basis for evaluating novel treatment strategies against acute lung injury.

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