• Journal of Physiology & Pathology in Korean Medicine
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• v.17 no.6
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• pp.1453-1462
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• 2003

In order to study the effect of oral administration of Mawhangyounpye-tang against to asthma, astham was induced to allergy-sensitive Balb/c mouse with ovalbumin using method of Hatfield et al (1997). The changes of diameter lumen of upper portion of the trachea, lung weight, gross appearance of lung, histological profiles of lung and trachea, numbers of cellular compartments in the bronchoalveolar lavage fluid (BALF), numbers and morphology of the mast cells in the trachea, numbers of mucus-secretory cell in the broncus, morphology of the bronchus, ultramicroscopical appearance of surface of trachea and number of cilia and mucous-secretory cells by scanning electron microscope. Obtained results were as follows. 1. The diameters of trachea lumen were significantly decreased in asthma induced control groups and these decreasing were result from hypertrophy of mucous membrane. However, these phenomena were dramatically recovered in the Mawhangyounpye-tang dosing groups. 2. Lung weights and black spots, which were result from infiltration of inflammatory cells, were significantly increased in asthma induced control groups but these phenomena were dramatically recovered in the Mawhangyounpye-tang dosing groups. 3. Hypertrophy of mucous membrane of trachea and bronchus and !bronchioles in the lung, peritracheal, peribronchus and peribronchiolar inflammatory cell infiltration, and mucoid exudate deposit in the lumen were observed in asthma induced control groups but these phenomena were dramatically recovered in the Mawhangyounpye-tang dosing groups. 4. Cellular compartments including neutrophil and eosinophil were dramatically increased in the BALF of asthma induced control groups but these phenomena were dramatically recovered in the Mawhangyounpye-tang dosing groups. 5. Mast cell degranulation and decreasing of the numbers of mast cells were detected in the trachea of asthma induced control groups. However, these phenomena were dramatically recovered in the Mawhangyounpye-tang dosing groups. 6. Shed, decreasing of cilia cell and increasing of mucous-secretory cells in the surface of the trachea of asthma induced control groups but these phenomena were dramatically recovered in the Mawhangyounpye-tang dosing groups. In conclusion, it Is considered that Mawhangyounpye-tang has somewhat favorable effect on the asthma because the asthma specific series of abnormalities in respiratory system were decreased after oral administratin of Mawhangyounpye-tang in this study. In future, it is needed that the toxicological and dosagespecific study of Mawhangyounpye-tang to use against asthma with safe.

• Journal of Microbiology and Biotechnology
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• v.27 no.9
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• pp.1628-1638
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• 2017

Viola tianshanica Maxim, belonging to the Violaceae plant family, is traditionally used in Uighur medicine for treating pneumonia, headache, and fever. There is, however, a lack of basic understanding of its pharmacological activities. This study was designed to observe the effects of the ethanol extract (TSM) from Viola tianshanica Maxim on the inflammation response in acute lung injury (ALI) induced by LPS and the possible underlying mechanisms. We found that TSM (200 and 500 mg/kg) significantly decreased inflammatory cytokine production and the number of inflammatory cells, including macrophages and neutrophils, in bronchoalveolar lavage fluid. TSM also markedly inhibited the lung wet-to-dry ratio and alleviated pathological changes in lung tissues. In vitro, after TSM ($12.5-100{\mu}g/ml$) treatment to RAW 264.7 cells for 1 h, LPS ($1{\mu}g/ml$) was added and the cells were further incubated for 24 h. TSM dose-dependently inhibited the levels of proinflammatory cytokines, such as NO, $PGE_2$, $TNF-{\alpha}$, IL-6, and $IL-1{\beta}$, and remarkably decreased the protein and mRNA expression of $TNF-{\alpha}$ and IL-6 in LPS-stimulated RAW 264.7 cells. TSM also suppressed protein expression of $p-I{\kappa}Ba$ and p-ERK1/2 and blocked nuclear translocation of $NF-{\kappa}B$ p65. The results indicate that TSM exerts anti-inflammatory effects related with inhibition on $NF-{\kappa}B$ and MAPK (p-ERK1/2) signaling pathways. In conclusion, our data demonstrate that TSM might be a potential agent for the treatment of ALI.

• Tuberculosis and Respiratory Diseases
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• v.39 no.2
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• pp.120-130
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• 1992

Background: Although there have been many studies on the pathogenetic mechanism of acute lung injury, it is still elusive. Recently interests have been focused on the role of oxygen free radicals. But the effect of hydroxyl radical on the neutrophil mobilization and the alveolar-capillary permeability is not clear especially in the endotoxin-induced acute lung injury model of rats. This investigation was performed to evaluate the pathogenetic role of hydroxyl radical on the neutrophil accumulation into the lung and the increased alveolar-capillary permeability in the endotoxin-induced acute lung injury in rats. Method: Fifty rats were divided into four groups: vehicle control group (n=5, 6hrs; n=5, 24hrs), endotoxin-treated group (n=10, 6hrs; n=10, 24hrs), Dimethylthiourea (DMTU)-pretreated group (n=10, 6hrs), and deferoxamine (DFX)-pretreated group (n=10, 6hrs). Thirty minutes before sacrifice, $^{125}I$-tagged bovine serum albumin was injected. Six and twenty four hours after endotoxin injection, the rats were sacrificed, and the radioactivity of lung tissue and peripheral blood was counted. Permeability index was defined as the ratio of radioactivity between lung tissue and peripheral blood. Another set of rats (n=52) were divided into the same four groups as before [vehicle control group (n=5, 6hrs; n=5, 24hrs), endotoxin·treated group (n=7, 6hrs; n=8, 24hrs), DMTU-pretreated group (n=6, 6hrs; n=9, 24hrs), and DFX-pretreated group (n=5, 6hrs; n=7, 24hrs)], and were sacrificed 6 and 24 hours after endotoxin injection. In these rats, cell profile of peripheral blood and bronchoalveolar lavage fluid was evaluated, and the pathologic examination of lung tissue was performed. Results: 1) Increased alveolar-capillary permeability was observed 6 hours after endotoxin injection, which was normalized after 24 hours, and this increase was attenuated by pretreatment with DMTU and DFX. 2) Neutrophil sequestration into the lung was observed 24 hours after endotoxin administration, but this was not influenced by DMTU and DFX pretreatment. Conclusion: These results suggest that hydroxyl radical would not be involved in the sequestration of neutrophils into the lung, but plays an important role in the increase of alveolar-capillary permeability in the endotoxin-induced acute lung injury in rats.

• Radiation Oncology Journal
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• v.18 no.4
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• pp.321-328
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• 2000

Purpose :NOS2 induce NO Production and NO activate TGF-${\beta}$. The TGF-${\beta}$ is a inhibitor of NOS2. If this negative feedback mechanism operating in radiation pneumonitis model, NOS2 inhibitor may play a role in TGF-${\beta}$ suppression. We planned this study to evaluate the expression patterns of NO, NOS2 and TGF-${\beta}$ in vivo radiation pneumonitis model. Materials and Methods : Sixty sprague-Dawley rat were irradiated 5 Gy or 20 Gy. They were sacrificed 3, 7, 14, 28 and 56 days after irradiation. During sacrifice, we peformed broncho-alveolar lavage (BAL). The BAL fluids were centrifuged and supernatents were used for measure NO and TGF-${\beta}$, and the cells were used for RT-PCR. Results : After 5 Gy of radiation, NO in BAL fluid increased at 28 days in both lung and TGF-${\beta}$ in left lung at 56 days. NO increased in BAL fluid at 28 days in both lung after irradiation and TGF-${\beta}$ in right lung at 28-56 days after 20 Gy of radiation. After 5 Gy of radiation, NOS2 expression was increased in right lung at 14 days, in both lung at 28 days and in left lung at 56 days. TGF-${\beta}$ expression was reduced in both lung at 28 days and increased in left lung at 56 days. Conclusions :The Proposed feedback mechanism of NO, NOS2 and TGF-${\beta}$ was operated in vivo radiation pneumonitis model. At 56 days, however, NOS2 and TGF-${\beta}$ expressed concurrently in left lung after 5 Gy and in both lung after 20 Gy of radiation.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.27 no.3
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• pp.84-95
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• 2014

Objective : Ephedra sinica (ES) has has been used as remedy of allergic diseases for a long time in Korea. In the present study, we investigated the anti-allergic effects of ES on experimental allergic asthma mouse model using ovalbumin (OVA). Methods : BALB/c mice were sensitized and challenged with 100 ug of OVA and 1 mg of aluminum potassium sulfate of 0.2 ml phosphate-buffered saline(PBS) intraperitoneally on day 1 and 15. mice were challenged on 3 consecutive days with 5% OVA and AHR was assessed 24 h after the last challenge. we examined the lung histology, airway hyper sensitivity, total inflammatory cell count in bronchoaveloar lavage fluid(BALF), Th2-associated cytokines production and IgE production. Results : ES potently inhibited the lung damage and the development of Penh. ES also reduced the number of BAL cells during OVA-induced allergic asthma. Furthermore, ES inhibited cytokines production such as IL-4, IL-13 productions, and IgE level of serum. Conclusion : These results suggest that ES may inhibit the production of IL-4, IL-13, IgE and infiltration of inflammatory cell and be beneficial oriental medicine for allergic asthma.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.27 no.3
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• pp.96-105
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• 2014

Objective : Glycyrrhiza uralensis Fisch (GUF) has been used as remedy of allergic diseases for a long time in Korea. In the present study, we investigated the anti-allergic effects of GUF on experimental allergic asthma mouse model using ovalbumin (OVA). Methods : BALB/c mice were sensitized and challenged with 100 ug of OVA and 1 mg of aluminum potassium sulfate of 0.2 ml phosphate-buffered saline (PBS) intraperitoneally on day 1 and 15. Mice were challenged on 3 consecutive days with 5% OVA and AHR was assessed 24 hrs after the last challenge. We examined total inflammatory cell number in bronchoaveloar lavage fluid (BALF), Th2-associated cytokine productions and lung histology. Results : GUF potently inhibited the development of airway hypersensitivity and also reduced the number of BAL cells during OVA-induced allergic asthma. GUF also inhibited cytokine productions such as IL-4, IL-13 in lung tissue. Furthermore, GUF treatment inhibited allergic airway inflammation. Conclusion : These results suggest that GUF may inhibit the production of IL-4, IL-13 and infiltration of inflammatory cell and be beneficial oriental medicine for allergic asthma.

• Journal of Environmental Health Sciences
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• v.43 no.4
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• pp.273-279
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• 2017

Objectives: Carbon nanotubes (CNTs) are next-generation industrial nanoparticles which possess excellent mechanical strength along with good thermal conductivity and electric properties. Given these characteristics, carbon nanotubes are being widely applied in various fields, including research and development. However, concerns have been raised over hazardous properties due to their similar fiber shape to asbestos. Recent studies have shown that CNTs pose potential hazards which may cause fibrosis and/or lung inflammation similarly to asbestos. Methods: After intratracheal instillation of SWCNTs and MWCNTs to rats, pulmonary surfactant (PS) of the SWCNTs and MWCNTs was measured and analyzed using bronchoalveolar lavage fluid collected from the lung. After a single intratracheal instillation of SWCNTs and MWCNTs, phospholipid predominantly showed a significant increase compared to the control group, while proteins exhibited a significant increase both three days and one week after instillation. Results: As a result of surface tension, MWCNTs showed a significant decrease three days after treatment compared to the control group. In the case of the total cell number three days after instillation, MWCNTs revealed a temporarily significant increase when compared to the control group. For PMN number, when compared to the control group, SWCNTs displayed a significant increase throughout the observation period, while MWCNTs showed a significant increase three days and three months after treatment. Conclusions: After exposure to CNTs, the total cell number and PNT number, which indicate inflammatory response, were significantly increased. Therefore, this study suggests fiber-shaped CNTs may have a harmful effect on the lungs.

• Toxicological Research
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• v.34 no.4
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• pp.343-354
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• 2018

Aluminum oxide nanoparticles ($Al_2O_3$ NPs) are among the most widely used nanomaterials; however, relatively little information about their risk identification and assessment is available. In the present study, we aimed to investigate the potential toxicity of $Al_2O_3$ NPs following repeated inhalation exposure in male Sprague-Dawley rats. Rats were exposed to $Al_2O_3$ NPs for 28 days (5 days/week) at doses of 0, 0.2, 1, and $5mg/m^3$ using a nose-only inhalation system. During the experimental period, we evaluated the clinical signs, body weight change, hematological and serum biochemical parameters, necropsy findings, organ weight, and histopathology findings. Additionally, we analyzed the bronchoalveolar lavage fluid (BALF), including differential leukocyte counts, and aluminum contents in the major organs and blood. Aluminum contents were the highest in lung tissues and showed a dose-dependent relationship in the exposure group. Histopathology showed alveolar macrophage accumulation in the lungs of rats in the $5mg/m^3$ group during exposure and recovery. These changes tended to increase at the end of the recovery period. In the BALF analysis, total cell and neutrophil counts and lactate dehydrogenase, tumor necrosis factor-${\alpha}$, and interleukin-6 levels significantly increased in the 1 and $5mg/m^3$ groups during exposure. Under the present experimental conditions, we suggested that the no-observed-adverse-effect level of $Al_2O_3$ NPs in male rats was $1mg/m^3$, and the target organ was the lung.

• Biomolecules & Therapeutics
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• v.26 no.6
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• pp.539-545
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• 2018

4-Hydroxy-2-(4-hydroxyphenethyl)isoindoline-1,3-dione (PD1) is a synthetic phthalimide derivative of a marine compound. PD1 has peroxisome proliferator-activated receptor (PPAR) ${\gamma}$ agonistic and anti-inflammatory effects. This study aimed to investigate the effect of PD1 on allergic asthma using rat basophilic leukemia (RBL)-2H3 mast cells and an ovalbumin (OVA)-induced asthma mouse model. In vitro, PD1 suppressed ${\beta}$-hexosaminidase activity in RBL-2H3 cells. In the OVA-induced allergic asthma mouse model, increased inflammatory cells and elevated Th2 and Th1 cytokine levels were observed in bronchoalveolar lavage fluid (BALF) and lung tissue. PD1 administration decreased the numbers of inflammatory cells, especially eosinophils, and reduced the mRNA and protein levels of the Th2 cytokines including interleukin (IL)-4 and IL-13, in BALF and lung tissue. The severity of inflammation and mucin secretion in the lungs of PD1-treated mice was also less. These findings indicate that PD1 could be a potential compound for anti-allergic therapy.

• Biomolecules & Therapeutics
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• v.26 no.6
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• pp.576-583
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• 2018

Human rhinoviruses (HRV) are one of the major causes of common cold in humans and are also associated with acute asthma and bronchial illness. Heat-shock protein 90 (Hsp90), a molecular chaperone, is an important host factor for the replication of single-strand RNA viruses. In the current study, we examined the effect of the Hsp90 inhibitor pochonin D, in vitro and in vivo, using a murine model of human rhinovirus type 1B (HRV1B) infection. Our data suggested that Hsp90 inhibition significantly reduced the inflammatory cytokine production and lung damage caused by HRV1B infection. The viral titer was significantly lowered in HRV1B-infected lungs and in Hela cells upon treatment with pochonin D. Infiltration of innate immune cells including granulocytes and monocytes was also reduced in the bronchoalveolar lavage (BAL) by pochonin D treatment after HRV1B infection. Histological analysis of the lung and respiratory tract showed that pochonin D protected the mice from HRV1B infection. Collectively, our results suggest that the Hsp90 inhibitor, pochonin D, could be an attractive antiviral therapeutic for treating HRV infection.