• Tuberculosis and Respiratory Diseases
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• 제82권4호
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• pp.311-318
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• 2019

Background: Although physical activity is known to be beneficial to lung function, few studies have been conducted to investigate the correlation between physical activity and lung function in dusty areas. Therefore, the purpose of this study is to investigate the correlation between physical activity and lung function in a Korean cohort including normal and COPD-diagnosed participants. Methods: Data obtained from the COPD in dusty areas (CODA) cohort was analyzed for the following factors: lung function, symptoms, and information about physical activity. Information on physical activity was valuated using questionnaires, and participants were categorized into two groups: active and inactive. The evaluation of the mean lung function, modified Medical Research Council dyspnea grade scores, and COPD assessment test scores was done based on the participant physical activity using a general linear model after adjusting for age, sex, smoking status, pack-years, height, and weight. In addition, a stratification analysis was performed based on the smoking status and COPD. Results: Physical activity had a correlation with high forced expiratory volume in 1 second ($FEV_1$) among CODA cohort (p=0.03). While the active group exhibited significantly higher $FEV_1$ compared to one exhibited by the inactive group among past smokers (p=0.02), no such correlation existed among current smokers. There was no significant difference observed in lung function after it was stratified by COPD. Conclusion: This study established a positive correlation between regular physical activity in dusty areas and lung function in participants.

• 대한통합의학회지
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• 제12권1호
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• pp.27-39
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• 2024

Purpose : Smoking is a major factor in chronic obstructive pulmonary disease (COPD), but the effect of electrical cigarette smoking on COPD development is still uncertain. This study aimed to compare the functions of airways and lungs exposed to combustible cigarettes and electrical cigarettes based on the pulmonary function test (PFT) results from the Korean National Health and Nutrition Examination Survey (NHANES). Methods : This study used data from 8,942 participants with PFT results out of 47,309 total subjects from the 6th to 8th Korean NHANES (2014-2015, 2016-2018, and 2019, respectively). Individuals with diseases such as cancer, ex-smokers, and dual tobacco users were excluded. The PFT results were analyzed according to the COPD diagnostic criteria. After adjusting for confounding variables, a complex sample generalized linear model ANOVA test was performed to investigate the association between PFT results and combustible smoker or electrical cigarette user groups. Results : In an analysis based on the obstructive ventilatory disorders (forced expiratory volume in 1 second[FEV₁]/forced vital capacity[FVC]<.7), combustible cigarette smokers showed a 3.46 times higher risk of COPD compared to non-smokers, while electrical cigarette smokers exhibited no significant difference in terms of COPD-related risks compared to non-smokers. FEV₁ showed a negative relation with combustible cigarette smokers as reported elsewhere (B=-.07, p<.001). FEV₁/FVC was negatively related to both combustible cigarette smokers (B=-.03, p<.001) and electrical cigarette smokers (B=-.02, p<.001). Conclusion : FEV₁/FVC decreases were observed in the long-term exposure to both combustible and electrical cigarettes. The lower FEV₁ in the combustible cigarette group implies the worsening of the severity of COPD, suggesting more damage to the airways and lungs in the short term. Therefore, the temporary electrical cigarettes use for the transition period in order to smoking cessation potentially aids to reduce the harmful effect of combustible cigarettes in COPD development.

• 대한한방내과학회지
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• 제45권1호
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• pp.11-30
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• 2024

Objectives: This study evaluated the effects of Ssanghwa-tang (SHT) on lung injury and muscle loss in a COPD mouse model. Methods: C57BL/6 mice were challenged with cigarette smoke extract and lipopolysaccharide, and then treated with two concentrations of SHT (250 and 500 mg/kg). After sacrifice, the bronchoalveolar lavage fluid (BALF) or lung tissue was analyzed by cytospin, ELISA, real-time PCR, flow cytometry analysis, and H&E and Masson's trichrome staining. The grip strength of COPD mice was measured using a grip strength meter. The running time of COPD mice was measured by a treadmill test. Muscle tissue of the quadriceps was stained with H&E and Masson's trichrome staining. Results: SHT significantly inhibited the increase in neutrophil numbers in BALF and significantly decreased immune cell activity in BALF and lung tissue. It also significantly inhibited the increase in TNF-α, IL-17, and MIP2 in BALF. Real-time PCR analysis revealed that the mRNA expression of TNF-α, IL-17, MIP2, and TRPV1 in lung tissue showed a significant decrease compared with the control group. Lung tissue damage was significantly reduced in the histological analysis. The grip strength and running time of the COPD mice showed a significant decrease compared with the control group. In histological staining, SHT was found to reduce the damage to muscle tissue. Conclusions: This study indicates that SHT can be used as a therapeutic agent for COPD patients by inhibiting lung injury and muscle loss.

• 대한한방내과학회지
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• 제38권3호
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• pp.353-366
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• 2017

Objective: This study aimed to use a mouse model to evaluate the effects of Gwaruhaengryeon-hwan (GHH) on chronic obstructive pulmonary disease (COPD) and particulate matter induced lung injury. Materials and Methods: The study was carried out in two ways (in vitro, in vivo). In vitro RAW 264.7 cells (mouse macrophage) were used and analyzed by flow cytometry, ELISA. In vivo lipopolysaccharide (LPS) and cigarette smoke solution (CSS), or coal, fly ash, diesel exhaust particle (CFD) challenged mice were used and its BALF was analyzed by ELISA, lung tissue by real-time PCR. Results: In vitro, GHH maintained an 80-100% rate of viability. So cytotoxicity was not shown. In the ELISA analysis with RAW 264.7 cells, GHH significantly decreased NO over $30{\mu}g/ml$. In the ELISA analysis, GHH significantly decreased $TNF-{\alpha}$, IL-6 over $300{\mu}g/ml$. In the COPD model, the GHH 200 mg/kg dosage group, the application of GHH significantly decreased the increasing of neutrophils, $TNF-{\alpha}$, IL-17A, MIP2, CXCL-1 in BALF, $TNF-{\alpha}$, $IL-1{\beta}$ mRNA expression in lung tissue and histological lung injury. In the CFD induced lung injury model, the GHH 200 mg/kg dosage group, the application of GHH significantly decreased the increase of neutrophils, $TNF-{\alpha}$, IL-17A, MIP2, CXCL-1 in BALF, MUC5AC, $TGF-{\beta}$ mRNA expression in lung tissue and histological lung injury. Conclusion: This study suggests the usability of GHH for COPD patients by controlling lung tissue injury.

• Molecules and Cells
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• 제39권10호
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• pp.728-733
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• 2016

Mesenchymal stem cells (MSCs) effectively reduce airway inflammation and regenerate the alveolus in cigarette- and elastase-induced chronic obstructive pulmonary disease (COPD) animal models. The effects of stem cells are thought to be paracrine and immune-modulatory because very few stem cells remain in the lung one day after their systemic injection, which has been demonstrated previously. In this report, we analyzed the gene expression profiles to compare mouse lungs with chronic exposure to cigarette smoke with non-exposed lungs. Gene expression profiling was also conducted in a mouse lung tissue with chronic exposure to cigarette smoke following the systemic injection of human cord blood-derived mesenchymal stem cells (hCB-MSCs). Globally, 834 genes were differentially expressed after systemic injection of hCB-MSCs. Seven and 21 genes, respectively, were up-and downregulated on days 1, 4, and 14 after HCB-MSC injection. The Hbb and Hba, genes with oxygen transport and antioxidant functions, were increased on days 1 and 14. A serine protease inhibitor was also increased at a similar time point after injection of hCB-MSCs. Gene Ontology analysis indicated that the levels of genes related to immune responses, metabolic processes, and blood vessel development were altered, indicating host responses after hCB-MSC injection. These gene expression changes suggest that MSCs induce a regeneration mechanism against COPD induced by cigarette smoke. These analyses provide basic data for understanding the regeneration mechanisms promoted by hCB-MSCs in cigarette smoke-induced COPD.

• Journal of Microbiology and Biotechnology
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• 제33권5호
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• pp.634-643
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• 2023

Chronic obstructive pulmonary disease (COPD), one of the leading causes of death worldwide, is caused by repeated exposure to harmful matter, such as cigarette smoke. Although Lilium longiflorum Thunb (LLT) has anti-inflammatory effects, there is no report on the fermented LLT bulb extract regulating lung inflammation in COPD. Thus, we investigated the protective effect of LLT bulb extract fermented with Lactobacillus acidophilus 803 in COPD mouse models induced by cigarette smoke extract (CSE) and porcine pancreas elastase (PPE). Oral administration of the fermented product (LS803) suppressed the production of inflammatory mediators and the infiltration of immune cells involving neutrophils and macrophages, resulting in protective effects against lung damage. In addition, LS803 inhibited CSE- and LPS-induced IL-6 and IL-8 production in airway epithelial H292 cells as well as suppressed PMA-induced formation of neutrophil extracellular traps in HL-60 cells. In particular, LS803 significantly repressed the elevated IL-6 and MIP-2 production after CSE and LPS stimulation by suppressing the activity of the nuclear factor kappa-light-chain-enhancer of activated B (NFκB) in mouse peritoneal macrophages. Therefore, our results suggest that the fermented product LS803 is effective in preventing and alleviating lung inflammation.

• 대한한의학회지
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• 제34권2호
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• pp.10-19
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• 2013

Objectives: In the present study, we evaluate the anti-inflammatory effect of Lonicerae Flos on cigarette-induced lung inflammatory responses in animal model of chronic obstructive pulmonary diseases (COPD). Methods: To inspect the effects of Lonicerae Flos, we evaluated Lonicerae Flos functions in vivo including immune cell profiles in bronchoalveolar lavage (BAL) fluid, cytokine production and tissue morphological changes. Results: Lonicerae Flos significantly inhibited immune cell infiltrations into the BAL fluid (neutrophils, macrophages, lymphocytes). TNF-${\alpha}$, and interleukin-6 (IL-6) were substantially decreased in the BAL fluid of Lonicerae Flos-treated mice compared with cigarette-exposed control mice. In addition, the hypertrophy of goblet cells in the epithelial cells was reduced in both Lonicerae Flos- and roflumilast-treated mice. Conclusions: The results of this study provide evidence that treatment with Lonicerae Flos exerts strong therapeutic effects against cigarette-induced lung inflammation in vivo. Therefore, this herbal medicine may represent a novel therapeutic agent for lung inflammation in general, as well as a specific agent for the treatment of COPD.

• 대한한의학방제학회지
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• 제23권2호
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• pp.171-187
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• 2015

Objective This study aimed to evaluate the effects of Sagan-tang (SGT) on COPD mouse model. Methods The study was carried out by two ways (in vitro, in vivo). In vitro RAW264.7 cells (mouse macrophage) were used and analysed by flow cytometry, ELISA, Western blot. In vivo LPS and CSS challenged mice were used and its BALF had been analysed by cytospin image, FACS, ELISA, lung tissue by real-time PCR. Results In vitro, SGT maintained 80-100% rate of viablilty on 10 ~ 500 ㎍/㎖ concentration. In ELISA analysis with RAW264.7 cells, SGT significantly decreased NO over 30 ㎍/㎖. In flow cytometry, SGT 100 ㎍/㎖ dosage group displayed a tendency for decrease ROS. In Western blot analysis, SGT 100 ㎍/㎖ dosage group decreased NF-κB. In ELISA analysis, SGT significantly decreased TNF-α, IL-6 over 200 ㎍/㎖. In vivo SGT 200 ㎎/㎏ dosage group, application of SGT significantly decreased increase of neutrophils, TNF-α, IL-6 in BALF, muc5AC, TGF-β, TNF-α, expression of mRNA in lung tissue and histological lung injury. Conclusion This Study suggests usability of SGT for COPD patients by controlling lung tissue injury.

• Molecules and Cells
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• 제46권9호
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• pp.558-572
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• 2023

Chronic obstructive pulmonary disease (COPD) will be the third leading cause of death worldwide by 2030. One of its components, emphysema, has been defined as a lung disease that irreversibly damages the lungs' alveoli. Treatment is currently unavailable for emphysema symptoms and complete cure of the disease. Hyaluronan (HA) and proteoglycan link protein 1 (HAPLN1), an HA-binding protein linking HA in the extracellular matrix to stabilize the proteoglycan structure, forms a bulky hydrogel-like aggregate. Studies on the biological role of the full-length HAPLN1, a simple structure-stabilizing protein, are limited. Here, we demonstrated for the first time that treating human alveolar epithelial type 2 cells with recombinant human HAPLN1 (rhHAPLN1) increased TGF-β receptor 1 (TGF-β RI) protein levels, but not TGF-β RII, in a CD44-dependent manner with concurrent enhancement of the phosphorylated Smad3 (p-Smad3), but not p-Smad2, upon TGF-β1 stimulation. Furthermore, rhHAPLN1 significantly increased sirtuins levels (i.e., SIRT1/2/6) without TGF-β1 and inhibited acetylated p300 levels that were increased by TGF-β1. rhHAPLN1 is crucial in regulating cellular senescence, including p53, p21, and p16, and inflammation markers such as p-NF-κB and Nrf2. Both senile emphysema mouse model induced via intraperitoneal rhHAPLN1 injections and porcine pancreatic elastase (PPE)-induced COPD mouse model generated via rhHAPLN1-containing aerosols inhalations showed a significantly potent efficacy in reducing alveolar spaces enlargement. Preclinical trials are underway to investigate the effects of inhaled rhHAPLN1-containing aerosols on several COPD animal models.

• Tuberculosis and Respiratory Diseases
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• 제42권3호
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• pp.342-350
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• 1995

연구배경: 만성폐쇄성폐질환 환자에서 기관지확장제 사용후 임상 증상의 호전을 보이는 경우에도 폐기능 검사상 $FEV_1$의 증가가 뚜렷하지 않은 경우가 종종 관찰된다. 이러한 현상은 만성폐쇄성폐질환 환자에서 $FEV_1$이 환기기능의 변화를 예민하게 반응하지 못하기 때문으로 알려져 있다. 만성폐쇄성폐질환 환자에서 기저 병태생리는 호기시 기도폐쇄이지만 결과적으로 흡기시 호흡시스템의 부하가 증가하는 것이다. 그러므로 기관지확장제로 인한 환기역학의 개선으로 임상 증상이 호전되는데 이는 흡기시 부하가 감소된 결과일 가능성이 있다. 이에 저자들은 기관지확장제에 대한 흡기시 환기역학의 반응을 보기 위한 연구를 시행하였다. 방법: 대상은 17명의 만성폐쇄성폐질환환자이며 이중 3명은 여자였고 14명은 남자였다. 나이는 45세에서 80세 사이였으며($65.5{\pm}9.4$세) 검사전 최근 2주사이에 급성악화의 병력이 없는 안정상태에 있었다. 먼저 안정상태에서 호기와 흡기의 노력성유량-기량곡선(Forced F1ow-volume Curve)을 측정한 후 salbutamol($Ventolin^{(R)}$) 용액 10mg을 jet nebulizer($Devilbiss^{(R)}$ model 646)를 이용하여 4분간 흡입후 15분 뒤 다시 각각 호기와 흡기의 노력성유량-기량곡선을 측정하였다. 결과: 17명 환자의 기관지확장제 홉입전 $FEV_1$은 $0.92{\pm}0.34L$($38.3{\pm}14.9%$), FVC는 $2.25{\pm}0.81L$($71.1{\pm}21.0%$), $FEV_1$/FVC%는 $43.1{\pm}14.5%$였다. 기관지확장제 흡입후 $FEV_1$, FVC, Peak Inspiratory Flow(PIF)의 증가는 각각 $0.15{\pm}0.13L$, $0.58{\pm}0.38L$, $1.0{\pm}0.56L/sec$ 였으며, 초기값에 대한 변화율은 각각 $17.0{\pm}14.3%$, $29.0{\pm}22.5%$, $37.5{\pm}16.7%$ 였다. PIF의 증가는 $FEV_1$ 증가의 2배이상 되었으며(p<0.001), 기관지 확장제 흡입후 $FEV_1$의 증가가 거의 없었던 3례에서도 PIF의 증가는 각각 35.0%, 44.0%, 55.2% 였다. 결론: 만성폐쇄성폐질환 환자에서 기관지확장제에 의한 환기역학의 호전은 호기의 지표보다 흡기의 지표가 더 예민하게 반영하는 것으로 보인다.