Objective To investigate the role of inflammatory factors like serumleptin, adiponectin,interleukin-6( IL-6) , and C-reactive protein ( CRP) in the systemic inflammatory response of smokinginduced COPD. Methods Thirty male Wistar rats were randomly divided into three groups, ie. a high-dose smoking group, a low-dose smoking group, and a control group. Serum leptin, adiponectin, IL-6, and CRP levels were measured by ABC-ELISA. Results The serum leptin and adiponectin levels in both smoking groups decreased significantly compared with the control group( P lt; 0. 05) , while the difference was not significant between the two smoking groups ( P gt; 0. 05) . The serum IL-6 and CRP levels in both smoking groups increased significantly compared with the control group( P lt; 0. 05) , which were higher in the highdosesmoking group than those in the low-dose smoking group( P lt;0. 05) . Conclusions Smoking increases the serum levels of IL-6 and CRP, but reduces the serum levels of leptin and adiponectin in rats. These results suggest that leptin, adiponectin, IL-6, and CRP may be involved in the systemic inflammatory response of smoking-induced COPD.
Objective To explore the ultrastructure characteristics of pulmonary arteries in smokers with normal lung function and with chronic obstructive pulmonary disease ( COPD) . Methods 33 patients who undertook surgery for peripheral lung cancer were collected. According to smoking history and pulmonary function, the patients were divided into three groups, ie. non-smokers with normal pulmonary function ( group A, n = 10) , smokers with normal pulmonary function ( group B, n = 13) , and smokers in stable phase of COPD ( group C, n = 10) . Normal lung tissues without cancer were sampled and observed under light and electric microscope. Results ①Compared with group A, the thickness of intimal layer of intra-acinar pulmonary muscular arteries of group B and C were significantly higher, the area of their lumenwas lower, and the proportion of their muscular arteries was higher( P lt; 0. 01) . ②Ultrastructure of small pulmonary arteries of group A showed that intimal layer was normal, so as to endothelial cells and smooth muscle cells. Collagen fiber was not increased. Ultrastructure observation of group B showed that endothelialcells were distorted, basal membrane was thick, and collagen fiber increased in vessels. Ultrastructure observation of group C showed that endothelial cells degenerated, vascular intima thickness increased, andsynthetic phenotype smooth muscle cells increased. ③ Smoking index was positively correlated with the proportion of muscular arteries and the proportion of intimal area( r =0. 464,0. 635, P lt;0. 05, respectively) ,and negatively correlated with the proportion of lumen area( r= - 0. 603, P lt;0. 05) . Conclusions Smokers with normal lung fuction and with COPD show the similar ultrastructural characterizations in endothelial cells, smooth muscle cells, and pulmonary arterial remodeling, which related closely to smoking.
Objective To investigate the effects of smoking intensity, duration and cessation on mRNA and protein expressions of matrix metalloproteinase-9 ( MMP-9) in tracheal epitheliumof rats, and the relationship between smoking or smoking cessation and airway remodeling in chronic obstructive pulmonary disease ( COPD) . Methods Forty Wistar rats were randomly divided into 5 groups, ie. a normal control group, a long termheavy smoking group, a short termheavy smoking group, a long termlight smoking group,and a smoking cessation group which was exposed to room air for 10 weeks after long term heavy smoking.The expressions of MMP-9 mRNA and protein in tracheal epithelium of rats were detected by in situ hybridization and munohistochemistry respectively. Results ( 1) The pathological changes of emphysema were observed in the lung tissue of every smoking rat, and were most sever in the long term heavy smoking group. ( 2) Compared with the normal control group [ ( 0. 88 ±0. 88) PU, ( 2. 80 ±1. 66) PU] , the expressions of MMP-9 mRNA and proteins in tracheal epithelium were remarkable elevated in the long term heavy smoking group [ ( 22. 01 ±2. 86) PU, ( 20. 81 ±2. 46) PU] , the short term heavy smoking group [ ( 14. 94 ±3. 46) PU, ( 13. 68 ±2. 00) PU] , the long term light smoking group [ ( 6. 92 ±2. 71) PU,( 8. 84 ±1. 80) PU] and the smoking cessation group [ ( 19. 00 ±3. 36) PU, ( 14. 82 ±1. 74) PU] ( P lt;0. 01) . Compared with the long term heavy smoking group, the expressions of MMP-9 in tracheal epithelium were decreased in other three smoking groups ( P lt; 0. 05) . Conclusions Smoking could increase the expression of MMP-9 in tracheal epithelium and cause trachea damage and remodeling with intensity and duration in rats. Smoking cessation could decrease the MMP-9 expression and alleviate trachea remodeling,suggesting its role in the prevention of COPD.
ObjectiveTo analyze the burden of digestive diseases attributed to smoking in China from 1990 to 2019 and forecast its change in the next 10 years. MethodsThe Global Burden of Disease database 2019 was used to analyze the burden of digestive diseases attributed to smoking in China from 1990 to 2019. Joinpoint regression model was used to analyze the time variation trend. A time series model was used to predict the burden of digestive diseases attributable to smoking over the next 10 years. ResultsIn 2019, there were 12 900 deaths from digestive diseases attributed to smoking in China, with a DALY of 398 600 years, a crude death rate of 0.91/100 000 and a crude DALY rate of 28.02/100 000. The attributed standardized mortality rate was 0.69 per 100 000, and the standardized DALY rate was 19.79 per 100 000, which was higher than the global level. In 2019, the standardized mortality rate and DALY rate of males were higher than those of females (1.48/ 100 000 vs. 0.11/ 100 000, 38.42/ 100 000 vs. 293/100 000), and the standardized rates of males and females showed a downward trend over time. In 2019, both mortality and DALY rates from digestive diseases attributed to smoking increased with age. ARIMA predicts that over the next 10 years, the burden of disease in the digestive system caused by smoking will decrease significantly. ConclusionFrom 1990 to 2019, the burden of digestive diseases attributed to smoking showed a decreasing trend in China, and the problem of disease burden is more serious in men and the elderly population. A series of effective measures should be taken to reduce the smoking rate in key groups. The burden of digestive diseases caused by smoking will be significantly reduced in the next 10 years.
ObjectiveTo investigate the influence of endoplasmic reticulum stress (ERS) on smoking-induced nucleus pulposus cells apoptosis and inflammatory response.MethodsBetween October 2016 and October 2018, 25 patients with cervical disc herniation receiving discectomy were collected and divided into smoking group (14 cases) and non-smoking group (11 cases). The baseline data of age, gender, herniated segment, and Pfirrmann grading showed no significant difference between the two groups (P>0.05). The obtained nucelus pulposus tissues were harvested to observe the cell apoptosis via detecting the apoptosis-related proteins (Caspase-3 and PRAP) by TUNEL staining and Western blot test. The nucleus pulposus cells were isolated and cultured with enzyme digestion, of which the third generation cells were used in follow-up experiments. Then, the expressions of inflammatory factors [interleukin 1β (IL-1β) and tumor necrosis factor α (TNF-α)] were detected by ELISA; the nuclear translocation of P65 was monitored by cell immunofluorescence staining. Furthermore, ERS-related proteins (GRP78 and CHOP) were detected by Western blot; and endoplasmic reticulum ultrastructure was observed under transmission electron microscope. To verify the regulatory effect of ERS, cells were pretreated by ERS specific inhibitor (4-PBA), then cell apoptosis and inflammatory response were tested.ResultsThe nucleus pulposus tissue observation showed that the cell apoptotic rate and the expressions of apoptosis-related proteins (Caspase-3 and PARP) were obviously higher in smoking group than in non-smoking group (P<0.05). The nucleus pulposus cells observation indicated that the expressions of the inflammatory factors (IL-1β and TNF-α) and the ERS-related proteins (GRP78 and CHOP) were also higher in smoking group than in non-smoking group (P<0.05). The results of cell immunofluorescence staining further confirmed that smoking stimulated nuclear translocation of P65 in nucleus pulposus cells. The ERS injury was much more serious in smoking group than in non-smoking group. Furthermore, after 4-PBA inhibiting ERS, the expressions of GRP78, CHOP, IL-1β, TNF-α, and P65 were significantly decreased (P<0.05), and flow cytometry results showed that cell apoptotic rate in smoking group was decreased, showing significant difference compared with the non-smoking group (P<0.05).ConclusionSomking can stimulate cell apoptosis and inflammatory response in nucleus pulposus cells via ESR pathway. Suppressing ESR may be a novel target to suspend smoking-induced intervertebral disc degeneration.
Objective To determine if the therapeutic response to an inhaled corticosteroid is attenuated in individuals with asthma who smoke.Methods 38 outpatients with chronic stable asthma who visited during March 2008 and January 2009 were enrolled in the study. 23 cases were nonsmokers and 15 cases were smokers. All of them were treated by daily inhaled budesonide, and β2 agonist when necessary.They were required to record symptoms and peak expiratory flow every day on an asthmatic diary card. Thepatients were followed 28 days. ACT score, asthma-symptom score, Asthma Control Test ( ACT) score,pulmonary function, and peak expiratory flow were compared between the non-smoking and the smoking asthmatic patients. Results All of the patients had statistically significant increases in ACT score, mean morning and night PEF, mean forced expiratory volume in 1 second, and a significant decrease in asthmasymptom score after budesonide treatment compared with before. There were significantly greater changes inany of these parameters in the non-smokers than in the smokers. Conclusions Active cigarette smoking impairs the efficacy of short term inhaled corticosteroid treatment in asthma. This finding has important implications for the management of patients with asthma who smoke.
Objective To investigate the clinical characteristics, short-term therapy outcome and survival in patients of lung cancer with different smoking status. Methods 3751 cases were enrolled and the differences in age, sex, pathological type, stage, treatment modality, efficiency and survival were compared according patients′smoking status. Results 1206 ( 32. 2% ) patients were never smokers and 2545 ( 67. 8% ) were smokers. 80. 3% male patients and 10. 5% female patients were smokers. Among never smoking lung cancer patients, proportion of female gender, adenocarcinoma, second primary neoplasm,advanced stages and non-operative treatment were high. In the smokers, much more COPD and pulmonary tuberculosis, squamous cancer and operative treatmentwere found. No statistical differences were detected in overall outcome and survival. Conclusions The clinical characters and treatmentmodalities of patients with lung cancer of different smoking status were significant different, but had the same survival. Patients’smoking status should be accountted into the diagnosis and treatment of lung cancer.
Objective To systematically review the effectiveness of short message intervention on smoking cessation. Methods Databases including PubMed, The Cochrane Library, EMbase, CBM were searched from inception to August 2016, to collect randomized controlled trials (RCTs) about short message service (SMS) for smoking cessation. Two reviewers independently screened literature, extracted data and assessed the risk of bias of included studies. Then meta-analysis was performed using Stata 12.0 software. Results A total of 14 RCTs involving 15 543 participants were included. The results of meta-analysis showed that, compared with the control group, no significant difference was found in self-reported three months continuous abstinence (RR=0.830, 95%CI 0.679 to 1.014, P=0.069), 30 day point quit rate (RR=0.878, 95%CI 0.687 to 1.122, P=0.076). However, there were significant differences in the self-reported 7-day point abstinence (RR=1.149, 95%CI 1.014 to 1.303, P=0.03), the CO biochemical verification abstinence (RR=0.571, 95%CI 0.357 to 0.914, P=0.020), and the average number of cigarettes smoked per day (SMD=–0.25, 95%CI –0.37 to –0.12, P<0.001). Conclusion The available evidence indicates that short message intervention has a better effect on short-term smoking cessation. Therefore, more long-term studies are needed to determine the association between SMS and quit smoking behavior.
Objective To explore the effect of smoking on pulmonary function parameters of male patients with chronic obstructive pulmonary disease (COPD) and to analyze the correlation between smoking and pulmonary function parameters. Methods From January 2014 to October 2015, the pulmonary function parameters of 223 male outpatients or hospitalized patients with COPD in the Department of Respiratory Medicine were retrospectively analyzed by using SPSS 17.0 software. The patients were randomly divided into smoking group (n=98), smoking cessation group (n=82) and non-smoking group (n=43). Results Various degrees of damage or abnormality of lung capacity, ventilatory function, gas exchange function and airway resistance (Raw) existed in the patients with COPD. Compared with smoking cessation group and non-smoking group, residual volume/ total lung capacity (RV/TLC) and Raw were significantly higher (P< 0.05), maximum ventilatory volume, ventilation reserve percent, forced vital capacity, the percent of first second forced expiratory volume compared its predicted value (FEV1%pred), maximum mid-expiratory flow (MMEF), forced expiratory flow 50%, forced expiratory flow 75% and diffusing capacity of carbon monoxide were significantly lower (P<0.05) in the smoking group. There was a negative relationship between MMEF, FEV1%pred and smoking index (r=–0.352, –0.381, P<0.05), and a positive relationship between Raw, RV/TLC and smoking index (r=0.403, 0.378, P<0.05). Conclusions Most of the male COPD patients smoke or used to smoke. Smoking leads to ventilation and gas exchange function decrease, small airway limitation aggravation, airway resistance and emphysema degree increase in COPD patients. Smoking index has a negative relationship with MMEF, FEV1%pred and a positive relationship with Raw and RV/TLC.
Objective To observe the levels of malonaldehyde (MDA) , interleukin-8 (IL-8) and tumor necrosis factor-α(TNF-α) in lung tissues of subjects with or without chronic obstructive pulmonary disease (COPD) , and investigate their roles in the the pathogenesis of COPD. Methods The content of MDA, IL-8 and TNF-αin lung tissues of smokers with COPD (n=9) , ex-smokers with COPD (n=8) , non-smokers with COPD (n=7) , healthy smokers (n=9) , healthy ex-smokers (n=8) and healthy nonsmokers (n=6) was measured with enzyme-linked immunosorbent assay ( ELISA) and corrected by creatinine. Results The levels of MDA, IL-8 and TNF-α in lung tissues of the COPD patients were significantly higher than those in the healthy subjects (Plt;0.05) , which were also significantly higher in the smokers when compared with the non-smokers (Plt;0.05) , whether suffering from COPD or not. In the COPD patients, not the levels of IL-8 but MDA and TNF-αin lung tissues of the smokers were significantly higher than those in the ex-smokers (Plt;0.05) ; whereas in the healthy cases, no statistical significance was revealed between the smokers and the ex-smokers on the levels of MDA and IL-8 in lung tissues except TNF-α( Pgt;0.05) . Conclusion The abnormal increase of MDA, IL-8 and TNF-αin lung tissues caused by chronic smoking may play an important role in the the pathogenesis of COPD.