• Tuberculosis and Respiratory Diseases
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• v.42 no.3
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• pp.267-276
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• 1995

• The Journal of the Korean life insurance medical association
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• v.18
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• pp.15-20
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• 1999

• 대한임상약리학회:학술대회논문집
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• 1996.12a
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• pp.26-26
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• 1996

• Clinical and Experimental Pediatrics
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• v.45 no.5
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• pp.568-574
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• 2002

• Tuberculosis and Respiratory Diseases
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• v.42 no.5
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• pp.635-645
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• 1995

• Journal of the Korean Chemical Society
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• v.46 no.3
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• pp.205-212
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• 2002

Bioactive compounds of Chung-pi methoxy flavonoids were isolated by column chromatography and preparative chromatography, and investigated on the smoothing effect for the tracheal smooth muscle of rats. The tracheal smooth muscles of rats were treated with acetylcholine ($ED_{50}:3${\times}$10^{-6}M$) and with chromatographic fractions. We found that six-methoxylated flavonoid (nobiletin) was the most active compound fro the smoothing effect of which the contracted tracheal smooth muscle was screened with further separated ethyl acetate fraction. This result shows how nobiletin and its analogues could be using as a promising drug of bronchial asthma.

• Clinical and Experimental Pediatrics
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• v.52 no.6
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• pp.680-688
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• 2009

Purpose : Cysteinyl leukotrienes are important proinflammatory mediators in asthma. Recently, it was suggested that a promoter polymorphism in the genes encoding for leukotriene C4 synthase (LTC4S), a key enzyme in the leukotriene synthetic pathway, and cysteinyl leukotriene receptor 1 (CysLTR1) might be associated with aspirin-intolerant asthma. We investigated whether polymorphisms in LTC4S and CysLTR1 genes or their interactions were associated with the asthma phenotype, lung function, or bronchial hyperreactivity (BHR) in Korean children. Methods : A total of 856 asthmatic children and 254 non-asthmatic controls were enrolled; a skin prick test, lung function test and bronchial provocation test were performed. Of those enrolled, 395 children underwent exercise challenge tests. The LTC4S A(-444)C and CysLTR1 T(＋927)C were genotyped by polymerase chain reaction-restriction fragment length polymorphism analysis. Results : Of those enrolled, 699 children were classified as having atopic asthma and 277 children, as having exercise-induced asthma (EIA). LTC4S and CysLTR1 polymorphisms were not associated with atopic asthma, EIA, or asthma per se. Lung function and BHR were not significantly different between the wild type (AA or TT) and the variant (AC＋CC or TC＋CC) genotypes in asthmatics, atopic asthmatics, and EIA (＋) asthmatics, while total eosinophil counts were higher in the variant type of LTC4S than in the wild type in atopic asthmatics. There were no associations between the gene-gene interactions of LTC4S and CysLTR1 genotypes and the asthma phenotypes. Conclusion : LTC4S A(-444)C and CysLTR1 T(＋927)C polymorphisms and their gene-gene interactions are not associated with asthma phenotype, lung function, or BHR in Korean children.

• Tuberculosis and Respiratory Diseases
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• v.46 no.5
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• pp.697-708
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• 1999

Background : Leukotriene (LT) $C_4$, $D_4$, and $E_4$, the main components of slow-reacting substance of anaphylaxis (SRS-A), have been suggested to play an important role in bronchial asthma such as antigen-induced bronchoconstriction, airway hyperreactivity, and pulmonary eosinophil accumulation. The purpose of this study was to evaluate the effects of treatment with the cysteinyl-LTs (cys-LTs) antagonist, pranlukast on allergen-induced guinea pig asthma model. Methods : Guinea pigs of treatment and placebo groups were sensitized by subcutaneous injection of ovalbumin(OVA) and challenged by inhalation of aerosolized OVA (1% weight/volume OVA). Normal control group did not sensitize with OVA. Oral ingestion of pranlukast and normal saline to the treatment and placebo groups was performed. In the treatment and placebo groups, airway resistance was measured before and after oral ingestion. Serum $LTC_4$ and eosinophilic infiltration of the bronchiolar and peribronchiolar tissues were measured after ingestion in the treatment and placebo groups. Results : Allergen-induced airway constriction developed in 20 (8 in treatment group, 12 in placebo group) among 35 guinea pigs. Airway resistance was significantly decreased at 3 and 6 minutes after OVA challenge in the pranlukast treatment group. In the placebo group, there was no difference of airway resistance between before and after saline ingestion. Serum $LTC_4$ levels showed 348.4 pg/ml in the treatment group, 373.9 pg/ml in the placebo group, and 364.4 pg/ml in the control group. There were no statistically significant difference between treatment and placebo group (p=0.232), and treatment and control group (p=0.501). Eosinophilic infiltrations in the peribronchiolar region per one-microscopic field ($\times$400 high power fields) demonstrated 7.06 in the treatment group, 19.2 in the placebo group, and 4.50 in the control group. There was significant decrement of eosinophilic infiltration in the treatment group which was compared with placebo group (p=0.001). Conclusion : These results demonstrate that pranlukast, a cys-LTs receptor antagonist, can attenuate allergen induced early-phase bronchoconstriction and eosinophilic infiltration in the bronchiolar tissues.

• Tuberculosis and Respiratory Diseases
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• v.45 no.1
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• pp.77-89
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• 1998

Background: Genetic and environmental factors are known to affect the incidence and severity of asthma. Stimulation of $\beta_2$-Adrenergic Receptor ($\beta_2$AR) results in smooth muscle relaxation, leading to decrease in resistance of airflow. The gene encoding the $\beta_2$AR has recently been seguenced. The $\beta_2$AR genotype at the polymorphic loci of codons 16, 27, 34, and 164 was known to cause changes in the amino acids. The relationships between the structure of the $\beta_2$AR and its functions are being elucidated. Purpose : The gene encoding the $\beta_2$AR was carried out to assess the frequency of polymorphisms in bronchial asthma, to determine wheather these polymorphisms have any relation to the severity, or nocturnal symptoms in bronchial asthma. Methods: The subjects studied were 103 patients with bronchial asthma, which consisted of 30 mild episodic, 32 mild persistent, 17 moderate, and 24 severe asthma patients. The polymorphisms of the $\beta_2$AR gene were detected by mutated allele specific amplification (MASA) method at the codons 16,27,34, and 164. Results: The most frequent polymorphism was arginine 16 to glycine. The other two polymorphisms, valine 34 to methionine and glutamine 27 to glutamic acid occured in 11 and 6 patients respectively. The polymorphism of threonine 164 to isoleucine was not found in our enrolled patients. The homozygous polymorphism of $\beta_2$AR gene was found in only arginine 16 to glycine (12.6%). The heterozygous polymorphisms of $\beta_2$AR gene were in arginine 16 to glycine, valine 34 to methionine, and glutamine 27 to glutamic acid, as 65.1 %,10.7%, and 5.8% respectively in asthma patients. The presence of agrginine 16 to glycine heterozygous or/and homozygous polymorphism was associated in severe asthma (p=0.015), but there was no association between the other three polymorphisms and the severity of asthma. The frequency of the $\beta_2$AR gene polymorphisms was no relation in nocturnal asthma as compared with non-nocturnal asthma. Conclusion: The arginine 16 to glycine polymorphism of the $\beta_2$AR gene is the most frequently found in asthma patients and association with severe asthma. But there was no association between the polymorphism of the $\beta_2$AR gene and nocturnal asthma.

• Tuberculosis and Respiratory Diseases
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• v.44 no.1
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• pp.146-153
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• 1997

Background : Chronic cough is commomly defined as a persistent or recurrent cough exceeding 3 week's duration. The prevalence of chroinc cough is reported to range from 14% to 23 % for nonsmoking adults. The post nasal drip syndrome has been determined to be the most common cause of chronic cough, followed by asthma, chronic bronchitis, gastroesophageal reflux and bronchiectasis. Cough can be the only manifestation of asthma. Bronchial provocation tests are useful in diagnosing cough variant asthma. We investigated the clinical or laboratory findings and the incidence of airway hyperresponsiveness and evaluated the etiology in patients with chronic cough. Method : We evaluated 46 patients with chronic cough. Methacholine challenge test were done. Results : The results were as follows : 1) Thirty - five percent(16/46) of the chronic cough patients and 44% of the post nasal drip syndrom(7/16) showed the positive responses to methacholine challenge test 2) The underlying causes of chronic cough were post nasal drip syndrome in 35%, bronchitis in 21.7%, cough-variant asthma in 17.4%, and unknown condition in 25.9%. 3) Airway hyperresponsiveness in chronic cough was not related to respiratory symptom, nasal symptom, post nasal drip, smoking, derangement of ventilatory function, atopy, or sinusitis. Conclusion : Airway hyperresponsivenss in patients with chronic cough increased in frequency when compaired with normal control, allergic rhinitis. Cough-variant asthma account for 17.4% of patients with chronic cough.