Jae-Won Lee

Asiatic acid inhibits pulmonary inflammation induced by cigarette smoke.

Asiatic acid (AA) is one of the major components of Titrated extract of Centella asiatica (TECA), which has been reported to possess antioxidant and anti-inflammatory activities. The purpose of this study was to investigate the protective effect of AA on pulmonary inflammation induced by cigarette smoke (CS). AA significantly attenuated the infiltration of inflammatory cells in bronchoalveolar lavage fluid (BALF) of CS exposure mice. AA also decreased ROS production and NE activity, and inhibited the release of proinflammatory cytokines in BALF. AA reduced the recruitment of inflammatory cells and MCP-1 expression in lung tissue of CS exposure mice. AA also attenuated mucus overproduction, and decreased the activation of MAPKs and NF-kB in lung tissue. Furthermore, AA increased HO-1 expression and inhibited the reduced expression of SOD3 in lung tissue. These findings indicate that AA effectively inhibits pulmonary inflammatory response, which is an important process in the development of chronic obstructive pulmonary disease (COPD) via suppression of inflammatory mediators and induction of HO-1. Therefore, we suggest that AA has the potential to treat inflammatory disease such as COPD.

Estimation of populations exposed to road traffic noise in districts of Seoul metropolitan area of Korea.

This study aims to model road traffic noise levels and estimate the human exposure at the 25 districts in the metropolitan Seoul, Republic of Korea. The SoundPLAN® Version 7.1 software package was used to model noise levels and simulated road traffic noise maps were created. The people exposed to daytime/nighttime road traffic noise were also estimated. The proportions of the population exposed to road traffic noise in major cities in the EU were also estimated and compared. Eight (8) districts show the exceeded rate (percentage of the exposed population exceeding the daytime standard) of 20% or more, and eleven (11) districts show 10%-20% and six (6) districts show less than 10%, which indicates considerable variation among districts. Two districts (Nowon-gu and Yangcheon-gu) show the highest exposure rate during the daytime (35.2%). For nighttime noise levels, fourteen (14) districts show the exceeded rate (percentage of exposed population exceeding the nighttime standard) over 30%. The average percentages of the exposed population exceeding the daytime/nighttime standards in Seoul and the EU were 16.6%/34.8% and 13.0%/16.1%, respectively. The results show that road traffic noise reduction measures should urgently be taken for the nighttime traffic noise in Seoul. When the grid noise map and the 3-D façade noise map were compared, the 3-D façade noise map was more accurate in estimating exposed population in citywide noise mapping.

Callicarpa japonica Thunb. attenuates cigarette smoke-induced neutrophil inflammation and mucus secretion.

ETHNOPHARMACOLOGICAL RELEVANCE Callicarpa japonica Thunb. (CJT) is traditionally used as an herbal remedy for the treatment of inflammatory diseases in Korea, China, and Japan. In this study, we evaluated the effects of C. japonica Thunb. (CJT) on the development of COPD using a Cigarette smoke (CS)-induced murine model and cigarette smoke condensate (CSC)-stimulated H292 cells, human pulmonary mucoepidermoid cell line. MATERIAL AND METHODS C. japonica Thunb. was isolated from the leaves and stem of C. japonica. The methanol extract profile was obtained by UPLC Q-TOF-MS analysis. In in vivo experiment, the mice received 1h of cigarette smoke for 10 days. C. japonica Thunb. was administered to mice by oral gavage 1h before cigarette smoke exposure for 10 days. In in vitro experiment, we evaluated the effect of C. japonica Thunb. on the expression of MUC5AC and proinflammatory cytokines in H292 cells stimulated with CSC. RESULTS CJT treatment effectively suppressed the infiltration of neutrophils, and decreased the production of ROS and the activity of neutrophil elastase in the bronchoalveolar lavage fluid (BALF) induced by CS. CJT also significantly attenuated production of proinflammatory cytokines such as IL-6 and TNF-α in the BALF, and reduced the infiltration of inflammatory cells and the production of mucus in lung tissue induced by CS. In in vitro experiments, CJT decreased the expression of MUC5AC and proinflammatory cytokines in CSC-stimulated H292 cells. Furthermore, CJT attenuated the phosphorylation of ERK induced by CSC in H292 cells. Taken together, CJT effectively reduced the neutrophil airway inflammation and mucus secretion induced by CS in murine model, and inhibited the expression of MUC5AC in CSC-stimulated H292 human lung cell line. These findings suggest that CJT has a therapeutic potential for the treatment of COPD.

Picroside II Attenuates Airway Inflammation by Downregulating the Transcription Factor GATA3 and Th2-Related Cytokines in a Mouse Model of HDM-Induced Allergic Asthma

Picroside II isolated from Pseudolysimachion rotundum var. subintegrum has been used as traditional medicine to treat inflammatory diseases. In this study, we assessed whether picroside II has inhibitory effects on airway inflammation in a mouse model of house dust mite (HDM)-induced asthma. In the HDM-induced asthmatic model, picroside II significantly reduced inflammatory cell counts in the bronchoalveolar lavage fluid (BALF), the levels of total immunoglobulin (Ig) E and HDM-specific IgE and IgG1 in serum, airway inflammation, and mucus hypersecretion in the lung tissues. ELISA analysis showed that picroside II down-regulated the levels of Th2-related cytokines (including IL-4, IL-5, and IL-13) and asthma-related mediators, but it up-regulated Th1-related cytokine, IFNγ in BALF. Picroside II also inhibited the expression of Th2 type cytokine genes and the transcription factor GATA3 in the lung tissues of HDM-induced mice. Finally, we demonstrated that picroside II significantly decreased the expression of GATA3 and Th2 cytokines in developing Th2 cells, consistent with in vivo results. Taken together, these results indicate that picroside II has protective effects on allergic asthma by reducing GATA3 expression and Th2 cytokine bias.

Anti-inflammatory effect of stem bark of Paulownia tomentosa Steud. in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages and LPS-induced murine model of acute lung injury

ETHNOPHARMACOLOGICAL RELEVANCE The leaves, bark, and flowers of Paulownia tomentosa Steud. have been widely used as a traditional medicine in East Asia to treat inflammatory and infectious diseases. AIM OF THE STUDY We investigated the protective effect of the methanol stem bark extract of P. tomentosa using an animal model of lipopolysaccharide (LPS)-induced acute lung injury (ALI). MATERIALS AND METHODS The UPLC Q-TOF-MS profiles for the methanol extract of P. tomentosa stem bark showed that verbascoside and isoverbascoside were the predominant compounds. Raw 264.7 cells were used for inhibitory effects of cytokine production in vitro. C57BL/6N mice were administered intranasally with LPS (10μg/per mouse) to induce ALI. H&E staining was used to evaluate histological changes in the lung. RESULTS Treatment with P. tomentosa stem bark extract (PTBE) suppressed the production of IL-6 and TNF-α in LPS-stimulated RAW 264.7 macrophages, and the recruitment of neutrophils and macrophages in the BALF of mice with LPS-induced ALI. PTBE also decreased the levels of reactive oxygen species (ROS) and pro-inflammatory cytokines in the BALF. PTBE reduced the levels of nitric oxide (NO) in the serum and of inducible nitric oxide synthase (iNOS) in the lung of ALI mice. PTBE also attenuated the infiltration of inflammatory cells and the expression of monocyte chemoattractant protein-1 (MCP-1) in the lung. In addition, PTBE suppressed the activation of NF-κB and the reduced expression of superoxide dismutase 3 (SOD3) in the lung. CONCLUSION The results suggest that PTBE has a protective effect on LPS-induced ALI.

NPS 2143, a selective calcium-sensing receptor antagonist inhibits lipopolysaccharide-induced pulmonary inflammation

NPS 2143, a novel and selective antagonist of calcium-sensing receptor (CaSR) has been reported to possess anti-inflammatory activity. In the present study, we examined the protective effect of NPS 2143 on lipopolysaccharide (LPS)-induced acute lung injury (ALI). NPS 2143 pretreatment significantly inhibited the influx of inflammatory cells and the expression of monocyte chemoattractant protein-1 (MCP-1) in the lung of mice with LPS-induced ALI. NPS 2143 decreased the levels of neutrophil elastase (NE) and protein concentration in the bronchoalveolar lavage fluid (BALF). NPS 2143 also reduced the production of inflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in the BALF and serum. In addition, NPS 2143 attenuated the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), and increased the activation of AMP-activated protein kinase (AMPK) in the lung. NPS 2143 also downregulated the activation of nuclear factor-kappa B (NF-κB) in the lung. In LPS-stimulated H292 airway epithelial cells, NPS 2143 attenuated the releases of IL-6 and MCP-1. Furthermore, NPS 2143 upregulated the activation of AMPK and downregulated the activation of NF-κB. These results suggest that NPS 2143 could be potential agent for the treatment of inflammatory diseases including ALI.

The Study for the Assessment of the Noise Map for the Railway Noise Prediction Considering the Input Variables

The noise map can be applied to predict the effect of noise and establish the noise reduction measure. But the predicted value in the noise map can vary depending on the input variables. Thus, we surveyed the several prediction models and analyzed the changes corresponding to the variables for obtaining the coherency and accuracy of prediction results. As a result, we know that the Schall03 and CRN model can be applied to predict the railway noise in Korea and the correction value, such as bridges correction, multiple reflection correction, curve correction must be used for reflecting the condition of the prediction site. Also, we know that the prediction guideline is an essential prerequisite in order to obtain the unified and accurate predicted value for railway noise.

Regression Analysis of an Excavator Sound Power Level

The noise emitted from an excavator has long been a cause of environmental disputes, while causing displeasure to the nearby residents. So, the ministry of environment adopted the construction machinery noise labeling system to encourage the construction machinery manufacturing companies to develop the low noise construction machinery voluntarily. But, as the quality of life improves, a growing number of people desire the comfortable and quite environment to live in. Under the situation, noise from the construction machinery has been a major cause for stress and complaints. When the noise dispute happened in the construction site, the sound pressure level of the construction machinery like a excavator was measured at the lot boundary of the noise victims residence to judge how much noise damage occur. But the sound pressure level of the construction machinery is measured differently according to the acoustic environment of construction site and the measuring position, respectively, which makes it difficulty to judge whether the noise damage occur or not. As the sound power level of noise source is not affected by the acoustic environment of construction site and the measuring position, if we use the information of the sound power level, it will be easy to judge whether the noise damage occur and to establish the soundproofing measures. Therefore, we derive the sound power level regression model of the excavator to judge whether the noise emitted from the excavator damages to residents near the construction site. Also, the sound power level regression model of the excavator drawn in this paper will help construction companies to plan the noise reduction program in the construction sites.

3,4,5-Trihydroxycinnamic acid attenuates lipopolysaccharide (LPS)-induced acute lung injury via downregulating inflammatory molecules and upregulating HO-1/AMPK activation

ABSTRACT The increase in inflammatory cytokines and chemokines is a common denominator in the pathogenesis of acute lung injury (ALI) which are involved in the influx of inflammatory cells and lung damage. The aim of the present study was to evaluate the protective effect of 3,4,5‐trihydroxycinnamic acid (THC) in lipopolysaccharide (LPS)‐induced ALI. THC efficiently decreased the mRNA expression of interleukin‐8 (IL‐8) in LPS‐stimulated A549 airway epithelial cells. THC induced heme oxygenase‐1 (HO‐1) expression in A549 cells. THC also increased the activation of AMP‐activated protein kinase (AMPK) in A549 cells and RAW264.7 macrophages. In LPS‐induced ALI in mice, THC significantly suppressed neutrophil influx and monocyte chemoattractant protein‐1 (MCP‐1) production in the bronchoalveolar lavage fluid (BALF). THC also attenuated the levels of neutrophil elastase (NE), tumor necrosis factor‐&agr; (TNF‐&agr;) and interleukin‐6 (IL‐6) in the BALF and serum. In addition, THC inhibited the expressions of inducible nitric oxide synthase (iNOS) and the activation of nuclear factor‐kappa B (NF‐&kgr;B) in the lung. These protective effects of THC were accompanied with HO‐1 induction and AMPK activation. Taken together, the present study clearly demonstrates that THC significantly attenuates the LPS‐induced ALI, suggesting that THC might be a valuable therapeutic adjuvant in airway inflammatory disorders. HighlightsTHC reduces the mRNA expression of IL‐8 in LPS‐stimulated A549 airway epithelial cells.THC inhibits the influx of neutrophils and macrophages in the BALF of ALI mice.THC decreases the levels of NE, TNF‐&agr; and IL‐6 in the BALF and serum.THC attenuates the recruitment of inflammatory cells and the production of MCP‐1 in the lung.THC downregulates the activation of NF‐&kgr;B and upregulates the activation of HO‐1 and AMPK in the lung.

Lignans Isolated From Flower Buds of Magnolia fargesii Attenuate Airway Inflammation Induced by Cigarette Smoke in vitro and in vivo

The flower buds of Magnolia fargesii, known traditionally as Xinyi, exert anti-inflammatory effects against inflammatory lung diseases such as COPD. Lignans isolated from Xinyi are an important group of plant-derived anti-inflammatory compounds. However, the mechanisms of action underlying their protective effects against COPD are not yet fully understood. Here, we showed that seven lignans (lignans 1–7) obtained from a CHCl3 fraction of Xinyi effectively suppress the inflammatory response in CSC-stimulated airway epithelial cells (in vitro) and in a mouse model of COPD established by exposure to CS and LPS. The CHCl3 fraction was found to inhibit CSC-induced IL-6 expression in human airway epithelial cells and to suppress the infiltration of inflammatory cells (neutrophils and macrophages) and secretion of inflammatory cytokines, such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in the mouse model. Similarly, each of the seven lignans isolated from the CHCl3 fraction also suppressed the infiltration of inflammatory cells (neutrophils and macrophages) and secretion of inflammatory mediators such as reactive oxygen species (ROS), TNF-α, and IL-6 in vivo. Notably, all lignan compounds significantly suppressed both extracellular signal-related kinase (ERK) and Akt phosphorylation levels in CSC-stimulated human lung mucoepidermoid carcinoma (NCI-H292) cells. Of these, lignan 1 (dimethylpinoresinol) inhibited the expression of CSC-induced inflammatory cytokines (IL-1β, -6, and -8) in vitro in a dose-dependent manner by suppressing the activation of epidermal growth factor receptor (EGFR) and its downstream effectors, including ERK and Akt, in NCI-H292 cells. Our results show that the lignans isolated from Xinyi may prevent airway inflammatory diseases through the suppression of EGFR and its downstream effectors.