• Journal of Chest Surgery
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• v.38 no.7 s.252
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• pp.461-467
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• 2005

Pleura, diaphragm, pericardial fat pad, intercostal muscles and omentum can be used to protect and revascularize the bronchial suture line of tracheal transplantation, lung transplantation and pulmonary resection. The purpose of the present study is to compare the influence of the pleura, diaphragm and omentum in survival of isolated tracheal segments in the experimental animals. Material and Method: Sprague-Dawley rats weighing 250- 350g were used. The animals were divided in three groups; the pleura, omentum and diaphragm. Following intraperitoneal anesthesia, endotracheal intubation was performed. Then the trachea was exposed. A three-ring sec- tion of cervical trachea was excised. The resected trachea was implanted at each sites. After 2 weeks, rats were sacrificed. Histopathological examination of the tracheal segments was performed. For comparison of each groups, histopathological viability of resected tracheal segment was scored by three tissue layers; epithelium, submucosa, and cartilage. The results were presented as average score. Result: In histopathological examination, submucosa and cartilage using tracheal segment necrosis scoring system. The pleural group showed well preserved tissue. There was minimal necrosis and inflammation compared with other groups. In the pleural group, tracheal necrosis scores were $2.17\pm0.983$at epithelium, $1.67\pm0.516$ at submucosa and $2.17\pm0.753$ at cartilage. At the omental group, scores were $1.00\pm0.00,\;1.60\pm0.548\;and\;1.80\m0.447$. In the diaphragmatic group, scores were $1.40:\pm0.894,\;2.40\pm0.547\;and\;2.20\pm0.447$. Total necrosis score were $6.00\pm1.789$ in the pleural group, $4.40\pm0.894$ in the omental group and $6.00\pm1.414$ in the diaphragmatic group. Conclusion: There were no significant viability differences in terms of total necrosis score for the viability of resected tracheal segment. But the best result was achieved in the omental group. Therefore, omental wrapping on tracheal graft site will be beneficial for the prevention of graft necrosis.

• Korean Journal of Plant Resources
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• v.24 no.2
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• pp.236-242
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• 2011

In this present study, we investigated the anti-oxidant activity, the inhibition ability of lipid peroxidation, and the protective effect of cow pulmonary epithelium (CPAE) cells under oxidative stress using green tea and 3 types of fermented teas of Jeju Island. To compare the physiological activity of non-fermented and 3 types of fermented teas, the fermented time was controlled with 0 hr. (non fermented tea, G), 12 hrs. (20% fermented tea, F20), 17 hrs. (50% fermented tea, F50) and 24 hrs. (80% fermented tea, F80), respectively. Scavenging ability on DPPH radicals of 80 ${\mu}g/mL$ concentration of F20 was similar to that of 50 ${\mu}M$ epigallocatechin gallate (EGCG) but it was stronger than those of G, F50 and F80. All extracts tested inhibited LDL oxidation but G and F20 inhibited LDL oxidation 25~30% more than F50 and F80 at 40 ${\mu}g/mL$ concentration which was similar to that of 50 ${\mu}M$ EGCG. We observed that the CPAE cells treated with the tea extracts had a significant increase in cell viability, especially the cells under oxidative stress with 1 mM $H_2O_2$ as compared with the control group (no treatment with tea extracts). These findings suggested that all tea extracts containing fermented tea had a protective effect on oxidative stressed CPAE cells through their free radical scavenging activity. It can be concluded that F20 extracted from 20% fermented tea has the most significant antioxidative effects that inhibit lipid peroxidation and protect the CPAE cells under oxidative stress.

• Tuberculosis and Respiratory Diseases
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• v.79 no.3
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• pp.143-152
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• 2016

Background: Idiopathic pulmonary fibrosis (IPF) is a progressive and lethal lung disease characterized by the accumulation of excessive fibroblasts and myofibroblasts in the extracellular matrix. The transforming growth factor ${\beta}1$ (TGF-${\beta}1$)-induced epithelial-to-mesenchymal transition (EMT) is thought to be a possible source of fibroblasts/myofibroblasts in IPF lungs. We have previously reported that apolipoprotein A1 (ApoA1) has anti-fibrotic activity in experimental lung fibrosis. In this study, we determine whether ApoA1 modulates TGF-${\beta}1$-induced EMT in experimental lung fibrosis and clarify its mechanism of action. Methods: The A549 alveolar epithelial cell line was treated with TGF-${\beta}1$ with or without ApoA1. Morphological changes and expression of EMT-related markers, including E-cadherin, N-cadherin, and ${\alpha}$-smooth muscle actin were evaluated. Expressions of Smad and non-Smad mediators and TGF-${\beta}1$ receptor type 1 ($T{\beta}RI$) and type 2 ($T{\beta}RII$) were measured. The silica-induced lung fibrosis model was established using ApoA1 overexpressing transgenic mice. Results: TGF-${\beta}1$-treated A549 cells were changed to the mesenchymal morphology with less E-cadherin and more N-cadherin expression. The addition of ApoA1 inhibited the TGF-${\beta}1$-induced change of the EMT phenotype. ApoA1 inhibited the TGF-${\beta}1$-induced increase in the phosphorylation of Smad2 and 3 as well as that of ERK and p38 mitogen-activated protein kinase mediators. In addition, ApoA1 reduced the TGF-${\beta}1$-induced increase in $T{\beta}RI$ and $T{\beta}RII$ expression. In a mouse model of silica-induced lung fibrosis, ApoA1 overexpression reduced the silica-mediated effects, which were increased N-cadherin and decreased E-cadherin expression in the alveolar epithelium. Conclusion: Our data demonstrate that ApoA1 inhibits TGF-${\beta}1$-induced EMT in experimental lung fibrosis.

• Tuberculosis and Respiratory Diseases
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• v.52 no.6
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• pp.616-626
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• 2002

Background : The present study was performed to further improve our understanding of molecular mechanisms involved in the activation of NFkB, a major transcriptional factor involved in the inflammatory response in the lung, by particulate matter in lung epithelial cells with an aerodynamic diameter of less than $2.5{\mu}m$(PM2.5). Materials and Methods : Immediate production of reactive oxygen species (ROS) and nitrogen species (RNS), with the PM2.5 induced expression of inducible nitric oxide synthase (iNOS), $I{\kappa}B$ degradation and $NF{\kappa}B$-dependent transcriptional activity, in 549 cells, were monitored. Addition, we also examined the effect of the iNOS inhibitor, L-N6-(1-iminoethyl) lysine hydrochloride (L-NIL), on the PM2.5-induced $NF{\kappa}B$ activation in A549 cells. Results : The rapid degradation of $I{\kappa}B$ and the increase of transcriptional activity of the $NF{\kappa}B$-dependent promotor were observed in A549 cells exposed to PM2.5. The immediate production of ROS in response to PM2.5 in A549 cells was not clearly detected, although immediate responses were observed in RAW264.7 cells. A 549 cells, cultured in the presence of PM2.5, produced an increase in NO, which was noticeably significant after 15 min of exposure with the expression of iNOS mRNA. The addition of L-NIL, an iNOS inhibitor, significantly inhibited the PM2.5-induced $I{\kappa}B$ degradation and the increase of the $NF{\kappa}B$-dependent transcriptional activity. Conclusion : These results suggest that PM2.5 stimulates the immediate production of RNS, leading to the activation of $NF{\kappa}B$ in the pulmonary epithelium.

• Journal of Life Science
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• v.16 no.5
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• pp.780-787
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• 2006

Asthma is a chronic inflammatory disorder of the airways, which characterized by bronchial hyperresponsiveness, reversible airflow limitation and respiratory symptoms. Internationally, the prevalence of asthma has been increased over last 3 decades. Recently, several studies of asthma have been reported with gradually increasing importance. To tesify the hypothesis that interleukin (IL)-4 and IL-10 may be an important determinant of the severity of airway inflammation, their expression was studied in mouse model of asthma. BALB/c mouse, IL-4 Knockout (KO) mouse and IL-10 KO mouse were sensitized with intraperitoneal injection of ovalbumin adsorbed to aluminum potassium sulfate, followed by challenges with intranasal ovalbumin on 3 consecutive days. The severity of pulmonary inflammation was assessed by eosinophilia in BAL fluid, number of total BAL cells, histopathological changes in lung tissues, and immunohistochemical staining against IL-4 and IL-10. In BAL fluid, the number of total cells was significantly increased in asthma induced mouse compare to the control. In asthma induced mouse, eosinophil was increased to 56% and neutrophil was 0.2%. In H &E stains, eosinophilic infiltration and epithelium hyperplasia were clearly noticed in asthma induced mouse. In immunohistochemical staining for IL-4 and IL-10, there was no positive reaction in control group. However, very strong reactions were appeared in asthma induced group. In this research, IL-4 and IL-10, which seem to play a central role in allergic asthma, KO mouse was utilized to test the causative relationship between airway inflammation and role of specific cytokine. Asthma induced IL-4 and IL-10 KO mice showed much decreased inflammatory reactions in the number of total BAL cells, in eosinophilic infiltration, and in immunohistochemical stains against diverse inflammatory proteins. These results suggest that IL-4 and IL-10 increase the asthmatic reactions in vivo mice model.

• Tuberculosis and Respiratory Diseases
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• v.40 no.3
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• pp.236-249
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• 1993

Background: Among the injurious agents to which the lung airspaces are constantly exposed are reactive species of oxygen. It has been widely believed that reactive oxygen species may be implicated in the etiology of lung injuries. In order to elucidated how this oxidant causes lung cell injury, we investigated the effects of exogenous $H_2O_2$ on alveolar epithelial barrier characteristics. Methods: Rat type II alveolar epithelial cells were plated onto tissue culture-treated polycarbonate membrane filters. The resulting confluent monolayers on days 3 and 4 were mounted in a modified Ussing chamber and bathed on both sides with HEPES-buffered Ringer solution. The changes in short-circuit current (Isc) and monolayer resistance (R) in response to the exogenous hydroperoxide were measured. To determine the degree of cellular catalase participation in protection against $H_2O_2$ injury to the barrier, experiments were repeated in the presence of 20 mM aminotriazole (ATAZ, an inhibitor of catalase) in the same bathing fluid as the hydroperoxide. Results: These monolayers have a high transepithelial resistance (>2000 ohm-$cm^2$) and actively transport $Na^+$ from apical fluid. $H_2O_2$(0-100 mM) was then delivered to either apical or basolateral fluid. Resulting indicated that $H_2O_2$ decreased Isc and R gradually in dose-dependent manner. The effective concentration of apical $H_2O_2$ at which Isc (or R) was decreased by 50% at one hour ($ED_{50}$) was about 4 mM. However, basolateral $H_2O_2$ exposure led to $ED_{50}$ for Isc (and R) of about 0.04 mM. Inhibition of cellular catalase yielded $ED_{50}$ for Isc (and R) of about 0.4 mM when $H_2O_2$ was given apically, while $ED_{50}$ for basolateral exposure to $H_2O_2$ did not change in the presence of ATAZ. The rate of $H_2O_2$ consumption in apical and basolateral bathing fluids was the same, while cellualr catalase activity rose gradually with time in culture. Conclusion: Our data suggest that basolateral $H_2O_2$ may affect directly membrane component (e.g., $Na^+,\;K^+$-ATPase) located on the basolateral cell surface. Apical $H_2O_2$, on the other hand, may be largely degraded by catalase as it passes through the cells before reaching these membrane components. We conclude that alveolar epithelial barrier integrity as measured by Isc and R are compromised by $H_2O_2$ being relatively sensitive to basolateral (and insensitive to apical) $H_2O_2$.