scholarly journals A Rat Model to Determine the Biomedical Consequences of Concurrent Ethanol Ingestion and Cigarette Smoke Exposure

2004 ◽  
Vol 28 (7) ◽  
pp. 1120-1128 ◽  
Author(s):  
Martha J. Gentry-Nielsen ◽  
Elizabeth Vander Top ◽  
Mary U. Snitily ◽  
Carol A. Casey ◽  
Laurel C. Preheim
Keyword(s):  
Cigarette Smoke ◽  
Rat Model ◽  
Smoke Exposure ◽  
Ethanol Ingestion ◽  
Cigarette Smoke Exposure

scholarly journals Effect of Simvastatin on 5-HT and 5-HTT in a Rat Model of Pulmonary Artery Hypertension

2015 ◽  
Vol 37 (5) ◽  
pp. 1712-1724 ◽  
Author(s):  
Xue Jiang ◽  
LinDong Yuan ◽  
Peng Li ◽  
Jia Wang ◽  
Pengyu Wang ◽  
...  
Keyword(s):  
Body Weight ◽  
Pulmonary Artery ◽  
Cigarette Smoke ◽  
Rat Model ◽  
Structural Damage ◽  
Inflammatory Cells ◽  
Pulmonary Artery Hypertension ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Mean Pulmonary Arterial Pressure

Background/Aims: To investigaterole of serotonin (5-HT) and serotonin transporter (5-HTT) in a rat model of cigarette smoke-induced pulmonary artery hypertension (PAH) and the effect of statins on regulating 5HT and 5-HTT. Methods: A rat model of COPD comorbid with PAH was established by cigarette smoke exposure with or without simvastatin administration. The smoking and the simvastatin plus smoking groups were exposed to cigarette smoke daily, and the latter received simvastatin at 5mg/kg, once a day. After 16 weeks of cigarette smoke exposure, body weight and mean pulmonary arterial pressure (mPAP) were measured, bronchoalveolar lavage (BAL) was performed, and lung tissues and blood samples were collected to determine cardiopulmonary pathology, physiological indices, blood levelof 5-HT and expression of 5-HTT in the lung. Results: In addition to alveolar structural damage (COPD-like injury), chronic cigarette smoke exposure lead to pulmonary artery remodeling and PAH as evidenced by significant elevation of mPAP, RVHI, WT%and WA%. Cigarette smoke exposure resulted in significant reduction in animal body weight, and simvastatin significantly prevented smoke-induced weight loss. The number of inflammatory cells in BALF was dramatically increased in smoke exposed rats, and simvastatin dampened the number of leukocytes, neutrophils, lymphocytes, and macrophages. In addition, circulating 5-HTand expression of 5-HTT in the lung were significantly increased in the smoked rats compared to control rats, and it was significantly reduced by simvastatin. Alteration of BALF inflammatory cells, 5-HT and 5-HTT was significantly correlated with changes of mPAP, RVHI, WT% and WA%. Conclusions: Cigarette smoke exposure could result in not only COPD, but also PAH, which may attribute to the alteration of blood 5-HT and lung tissue 5-HTT. Simvastatin could significantly inhibited 5-HT and 5-HTT expression, and by which mechanism, it may protect animals from development of PAH.

Morphologic and Biomechanical Changes of Thoracic and Abdominal Aorta in a Rat Model of Cigarette Smoke Exposure

2013 ◽  
Vol 27 (6) ◽  
pp. 791-800 ◽  
Author(s):  
Rodrigo Gibin Jaldin ◽  
Édson Castardelli ◽  
Juliana Elaine Perobelli ◽  
Winston Bonetti Yoshida ◽  
Antônio de Castro Rodrigues ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Abdominal Aorta ◽  
Rat Model ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Biomechanical Changes ◽  
Thoracic And Abdominal

scholarly journals Effect of hydrogen inhalation on IL-40 and SIgA in a Rat Model of Pulmonary Mucosal Immunity

2020 ◽  
Author(s):  
Yiping Ma ◽  
Zhu Li ◽  
Yalei Zhao ◽  
Mo Sun ◽  
Wuzhuang Sun ◽  
...  
Keyword(s):  
Protein Expression ◽  
Cigarette Smoke ◽  
Rat Model ◽  
Airflow Obstruction ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Chronic Obstructive ◽  
Lung Pathology ◽  
Airway Wall ◽  
Tgf Β1

AbstractBackgroundRecently, some researchers have reported that PIgR expression is down-regulated in Chronic Obstructive Pulmonary Disease (COPD) and SIgA deficiency correlates with severity of airflow obstruction. What’ s more, some studies have demonstrated that 2 percent of hydrogen or hydrogen water is effective in treating and preventing various diseases.ObjectivesThe aim of this study was to observe the effect of hydrogen on the expression of SIgA, PIgR, IL-4, IL-5, TGF-β1 and IL-40 in lung tissue of COPD rats, to study the relationship between lung pathology parameter and SIgA, PIgR, therefore we can understand the effect of hydrogen on the development of COPD by changing SIgA expression of airway mucosal in COPD rats.MethodsA rat model of COPD was established by cigarette smoke exposure, and different concentrations of hydrogen were inhaled as intervention measures. After 4 months of cigarette smoke exposure, pathologic changes and airway wall remodeling of the lung were assessed by optical microscope. The protein expressions of SIgA, PIgR, IL-4, IL-5, TGF-β1 as well as IL-40 in the lung tissues were observed by immunohistochemistry or Western blot. The correlation between lung pathology parameter and the expression of SIgA, PIgR was analyzed. The correlation between SIgA and the expression of IL-4, IL-5, TGF-β1 and IL-40 was analyzed.ResultsThe results showed that hydrogen inhalation significantly ameliorated lung pathology and airway wall remodeling, increased the protein expression of SIgA, PIgR, IL-4, IL-5, and IL-40, and reduced the protein expression of TGF-β1.ConclusionsInhalation of 22% and 41.6% hydrogen showed a better effect than inhalation of 2% hydrogen. Hydrogen inhalation can significantly improve the expression of SIgA on the mucosal surface of COPD rats, which may be one of the mechanisms which hydrogen works on COPD pathogenesis.

Cigarette smoke exposure induces substantial changes in the airway epithelium of a Drosophila COPD model

Pneumologie ◽  
2016 ◽  
Vol 70 (07) ◽  
Author(s):  
M Thiedmann ◽  
R Prange ◽  
A Bhandari ◽  
K Kallsen ◽  
C Fink ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Airway Epithelium ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure
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