• The Korean Journal of Physiology and Pharmacology
• /
• v.22 no.5
• /
• pp.481-491
• /
• 2018

Allergic asthma is one of the most enduring diseases of the airway. The T-helper cells and regulatory T-cells are critically involved in inflammatory responses, mucus hypersecretion, airway remodelling and in airway hyper-responsiveness. Cigarette smoke (CS) has been found to aggravate inflammatory responses in asthma. Though currently employed drugs are effective, associated side effects demand identification and development of novel drugs with negligible or no adverse effects. Rutin, plant-derived flavonoid has been found to possess antioxidant and anti-inflammatory effects. We investigated the ability of rutin to modulate T-cells and inhibit inflammation in experimentally-induced asthma in cigarette smoke exposed mice. Separate groups of neonatal mice were exposed to CS for 10 days from post-natal days 2 to 11. After 2 weeks, the mice were sensitized and challenged with ovalbumin (OVA). Treatment group were given rutin (37.5 or 75 mg/kg body weight) during OVA sensitization and challenge. Rutin treatment was found to significantly inhibit cellular infiltration in the airways and Th2 and Th17 cytokine levels as well. Flow cytometry revealed effectively raised $CD4^+CD25^+Fox3^+$ Treg cells and supressed Th17 cell population on rutin treatment. Airway hyper-responsiveness observed following CS and OVA challenge were inhibited by rutin. $NF-{\kappa}B$ and iNOS, chief regulators of inflammatory responses robustly activated by CS and OVA were down-regulated by rutin. Rutin also inhibited the expression of matrix metalloproteinase 9, thereby aiding in prevention of airway remodelling in asthma thereby revealing to be a potent candidate in asthma therapy.

• Journal of Preventive Medicine and Public Health
• /
• v.50 no.1
• /
• pp.60-65
• /
• 2017

Objectives: We examined the prevalence of tobacco use and exposure to secondhand smoke among middle-school students in Korea using the Global Youth Tobacco Survey (GYTS) in 2013. Methods: The GYTS in Korea was conducted between July and August 2013 by the Korea Centers for Disease Control and Prevention. Data were collected using a self-administered anonymous questionnaire from a nationally representative sample of middle-school students aged 13-15 years in sampled classrooms. Results: The GYTS in Korea was completed by 4235 students aged 13-15 years in 43 middle schools. Approximately one in five of the students (17.8%) reported that they had tried cigarettes in the past, while 5.2% reported currently being cigarette smokers. Current cigarette smoking was higher in boys (7.5%) than in girls (2.6%). Of the students, 29.7% had been exposed to secondhand smoke at home, 47.4% inside enclosed public places, and 53.9% in outdoor public places. Of the current cigarette smokers, 25.7% bought their cigarettes from a store despite a law prohibiting this. Additionally, 58.0% of students noticed point-of-sale tobacco advertisements or promotions, 66.8% of current cigarette smokers wanted to stop smoking, and 70.9% of students had been taught about the dangers of tobacco use in school. Conclusions: These findings provide an opportunity to develop, implement, and evaluate a comprehensive tobacco control policy. The results suggest that youth have relatively easy access to cigarettes and are regularly exposed to secondhand smoke in public places, as well as to point-of-sale tobacco advertisements and promotions. Strict enforcement of the ban on tobacco sales to youth, expanding smoke-free areas, and advertising bans are needed to reduce tobacco use among youth.

• Journal of Ginseng Research
• /
• v.48 no.2
• /
• pp.181-189
• /
• 2024

Background: Cigarette smoke is generally accepted as a major contributor to chronic obstructive pulmonary disease (COPD), which is characterized by emphysematous lesions. In this study, we investigated the protective effects of Korean Red Ginseng (KRG) against cigarette smoke condensate (CSC)-induced emphysema. Methods: Mice were instilled with 50 mg/kg of CSC intranasally once a week for 4 weeks, KRG was administered to the mice once daily for 4 weeks at doses of 100 or 300 mg/kg, and dexamethasone (DEX, positive control) was administered to the mice once daily for 2 weeks at 3 mg/kg. Results: KRG markedly decreased the macrophage population in bronchoalveolar lavage fluid and reduced emphysematous lesions in the lung tissues. KRG suppressed CSC-induced apoptosis as revealed by terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick-end labeling staining and Caspase 3 immunohistochemistry. Additionally, KRG effectively inhibited CSC-mediated activation of Bcl-2-associated X protein/Caspase 3 signaling, followed by the induction of cell survival signaling, including vascular endothelial growth factor/phosphoinositide 3-kinase/protein kinase B in vivo and in vitro. The DEX group also showed similar improved results in vivo and in vitro. Conclusion: Taken together, KRG effectively inhibits macrophage-mediated emphysema induced by CSC exposure, possibly via the suppression of pro-apoptotic signaling, which results in cell survival pathway activation. These findings suggest that KRG has therapeutic potential for the prevention of emphysema in COPD patients.

• Asian Pacific Journal of Cancer Prevention
• /
• v.15 no.24
• /
• pp.10937-10941
• /
• 2015

Pathogenesis of lung cancer is a complicated biological process including multiple genetic and epigenetic changes. Since cigarette smoking is confirmed as the most main risk factor of non-small cell lung cancer (NSCLC), the aim of this study was to determine whether tobacco exposure plays a role in gene methylation. Methylation of the RAR-${\beta}$ gene were detected using methylation-specific polymerase chain reaction in DNA from 167 newly diagnosed cases with NSCLC and corresponding 105 controls. A significant statistical association was found in the detection rate of the promoter methylation of RAR-${\beta}$ gene between NSCLC and controls ($x^2$=166.01; p<0.01), and hypermethylation of the RAR-${\beta}$ gene was significantly associated with smoking status (p=0.038, p<0.05). No relationship was found between RAR-${\beta}$ gene methylation and pathologic staging including clinical stage, cell type, gender and drinking (p>0.05), and the methylation of RAR-${\beta}$ gene rate of NSCLC was slightly higher in stages III+IV (80.0%) than in I+II (70.8%). Similar results were obtained for methylation of the RAR-${\beta}$ gene between squamous cell carcinoma (77.9%) and other cell type lung cancer (73.9%). These results showed that the frequency of methylation increased gradually with the development of clinical stage in smoking-associated lung cancer patients, and tobacco smoke may be play a potential role in RAR-${\beta}$ gene methylation in the early pathogenesis and process in lung cancer, particularly squamous cell carcinoma. Aberrant promoter methylation is considered to be a promising marker of previous carcinogen exposure and cancer risk.

• Asian Pacific Journal of Cancer Prevention
• /
• v.14 no.12
• /
• pp.7725-7730
• /
• 2013

Objective: The purpose of this study was to evaluate secondhand smoke (SHS) exposure inside selected public places to provide basic data for the development and promotion of smoke-free policies. Methods: Between March and May 2009, an SHS exposure survey was conducted. $PM_{2.5}$ levels and air nicotine concentrations were measured in hospitals (n=5), government buildings (4), restaurants (10) and entertainment venues (10) in Seoul, Republic of Korea, using a common protocol. Field researchers completed an observational questionnaire to document evidence of active smoking (the smell of cigarette smoke, presence of cigarette butts and witnessing people smoking) and administered a questionnaire regarding building characteristics and smoking policy. Results: Indoor $PM_{2.5}$ levels and air nicotine concentrations were relatively higher in monitoring sites where smoking is not prohibited by law. Entertainment venues had the highest values of $PM_{2.5}$(${\mu}g/m^3$) and air nicotine concentration(${\mu}g/m^3$), which were 7.6 and 67.9 fold higher than those of hospitals, respectively, where the values were the lowest. When evidence of active smoking was present, the mean $PM_{2.5}$ level was 104.9 ${\mu}g/m^3$, i.e., more than 4-fold the level determined by the World Health Organization for 24-hr exposure (25 ${\mu}g/m^3$). Mean indoor air nicotine concentration at monitoring sites with evidence of active smoking was 59-fold higher than at sites without this evidence (2.94 ${\mu}g/m^3$ vs. 0.05 ${\mu}g/m^3$). The results were similar at all specific monitoring sites except restaurants, where mean indoor $PM_{2.5}$ levels did not differ at sites with and without active smoking evidence and indoor air nicotine concentrations were higher in sites without evidence of smoking. Conclusion: Nicotine was detected in most of our monitoring sites, including those where smoking is prohibited by law, such as hospitals, demonstrating that enforcement and compliance with current smoke-free policies in Korea is not adequate to protect against SHS exposure.

• Journal of the Korean Society of Tobacco Science
• /
• v.15 no.1
• /
• pp.3-14
• /
• 1993

Oxidants in environment or cigarette smoke are known to be implicated in the oxidative damages of pulmonary system. Such cellular damages are prevented by the presence of adequate levels of antioxidants in the tissue. In the present study, we investigated the influences of smoking duration and concentration of smoke on lung antioxidant defense in rats. Subchronic exposure of rats to smoke generated from 6 cigarettes per day for 90 days caused the activities of catalase and superoxide dismutase (SOD) to increase. However, glutathione peroxidase (GP-Xase) was not significantly changed. Total sulfhydryl compounds (Total-SH) in the lung homogenates from the rats inhaled with cigarette smoke for 15 days was decreased by 44% , thereafter it was returned to the level of normal rats. On the contrary, when rats were daily exposed to a different concentration of smoke generated from 1 to 20 cigarettes per day for 15 days, the activity of catalase was increased gradually with dose, but total SOD activity was increased only in the rats of low dose groups less than 5 cigarettes. Three types of SOD (one Cu, Zn-SOD with pI 4.9, and two Zn-SOD with pI 4.7 and 7.9)were detected in the lung homogenates and Zn-SOD with pI 4.7 was the major and cigarette-smoke inducible form. These results indicate that the protection of lung against oxidants from cigarette smoke seems to be accomplished by the induction of catalase and SOD, especially a cyanide resistant Zn-SOD with pI 4.f, following the consumption of antioxidants such as GSH in the beginning of inhalation period.

• Journal of Preventive Medicine and Public Health
• /
• v.43 no.1
• /
• pp.73-83
• /
• 2010

Objectives: We investigated the clustering of selected lifestyle factors (cigarette smoking, heavy alcohol consumption, lack of physical exercise) and identified the population characteristics associated with increasing lifestyle risks. Methods: Data on lifestyle risk factors, sociodemographic characteristics, and history of chronic diseases were obtained from 7,694 individuals ${\geq}20$ years of age who participated in the 2005 Korea National Health and Nutrition Examination Survey (KNHANES). Clustering of lifestyle risks involved the observed prevalence of multiple risks and those expected from marginal exposure prevalence of the three selected risk factors. Prevalence odds ratio was adopted as a measurement of clustering. Multiple correspondence analysis, Kendall tau correlation, Man-Whitney analysis, and ordinal logistic regression analysis were conducted to identify variables increasing lifestyle risks. Results: In both men and women, increased lifestyle risks were associated with clustering of: (1) cigarette smoking and excessive alcohol consumption, and (2) smoking, excessive alcohol consumption, and lack of physical exercise. Patterns of clustering for physical exercise were different from those for cigarette smoking and alcohol consumption. The increased unhealthy clustering was found among men 20-64 years of age with mild or moderate stress, and among women 35-49 years of age who were never-married, with mild stress, and increased body mass index (>$30\;kg/m^2$). Conclusions: Addressing a lack of physical exercise considering individual characteristics including gender, age, employment activity, and stress levels should be a focus of health promotion efforts.

• Asian Pacific Journal of Cancer Prevention
• /
• v.14 no.11
• /
• pp.6643-6647
• /
• 2013

Background: Despite the fact that breast cancer is the most common female cancer worldwide, more than half of the breast cancer risk factors remained unexplained. The aim of this study was to investigate the association of cigarette smoking with risk of breast cancer. Materials and Methods: A case-control study was conducted in the Clinical Centre of Kragujevac, Serbia, covering 382 participants (191 cases and 191 controls). In the analysis of data logistic regression was used. Results: Breast cancer risk was significantly increased in those who quit smoking at ${\leq}50$ years of age (OR=2.72; 95% confidence interval - 95%CI=1.02-7.27) and in those who quit smoking less than 5 years before diagnosis of the disease (OR=4.36; 95%CI=1.12-16.88). When smokers were compared with nonsmokers without passive exposure to smoking, former smoking significantly increased breast cancer risk (OR=2.37; 95%CI=1.07-5.24). Risk for breast cancer was significantly increased in those who quit smoking at ${\leq}50$ years of age (OR=3.29; 95%CI=1.17-9.27) and in those who quit smoking less than 5 years before diagnosis of the disease (OR=5.46; 95%CI=1.34-22.28). Conclusions: These data suggest that cigarette smoking is associated with an elevated risk of breast cancer among former smokers in Serbia.

• Journal of The Korean Society of Clinical Toxicology
• /
• v.18 no.2
• /
• pp.51-56
• /
• 2020

Purpose: Acute nicotine poisoning by liquid nicotine in electronic cigarettes is becoming an increasing problem worldwide. The current systematic review aimed to determine the harm of acute nicotine poisoning by reviewing published case reports. Methods: An online literature search with PubMed, Embase, Cochrane Library, and KoreaMed database was performed to identify relevant studies addressing acute nicotine poisoning with electronic cigarettes. Two investigators searched the case reports written in English or Korean. Results: Twenty-six cases were included in this study. The routes of intoxication included ingestion in 18 cases, intravenous injection in three cases, subcutaneous injection in two cases, and ocular exposure in two cases. Ten cases had a cardiac arrest, and seven of them died. Seven out of 12 cases with intentional poisoning had a cardiac arrest. Nine children under 18 years were reported, and three of them had a cardiac arrest. Sixteen cases without a cardiac arrest recovered well, except for one case with sudden sensorineural hearing loss. Conclusion: The authors reviewed the risks of electronic cigarette liquid in terms of acute poisoning through a systematic review. The nicotine solution of an e-cigarette can be life-threatening in cases of acute poisoning. Therefore, active emergency treatment with early recognition is necessary. In addition, various management methods and regulations for preventing acute nicotine poisoning, such as restriction of distribution and nicotine concentration, should be considered.

• The Journal of Korean Medicine
• /
• v.39 no.4
• /
• pp.126-135
• /
• 2018

Objectives: Chronic obstructive pulmonary disease (COPD) is characterized by chronic inflammation and irreversible airflow. This study aimed to evaluate the effects of GHX02 in a COPD-induced mouse model. Methods: The COPD mouse model was established by exposure to cigarette smoke extract and lipopolysaccharide which were administered by intratracheal injection three times with a 7 day interval. GHX02 (100, 200, 400 mg/kg) and all other drugs were orally administrated for 14 days from Day 7 to Day 21. Results: GHX02 significantly decreased the neutrophil counts in bronchoalveolar lavage fluid (BALF) and the number of $CD4^+$, $CD8^+$, $CD69^+$, and $CD11b^+/GR1^+$ cells in BALF and lung cells. GHX02 also suppressed the secretion of tumor necrosis factor-alpha ($TNF-{\alpha}$), interleukin-17A, macrophage inflammatory protein 2 (MIP2), and chemokine (C-X-C motif) ligand 1 (CXCL-1) in BALF and ameliorated the lung pathological changes. Conclusions: Thus, GHX02 effectively inhibited airway inflammation by inhibiting migration of inflammatory cells and expression of pro-inflammatory cytokines. Therefore, GHX02 may be a promising therapeutic agent for COPD.