The Prevalence, Pattern, and Factors Affecting Cigarette Smoking among Undergraduate Students in a Tertiary Institution in Plateau State, Nigeria

Background: Cigarette smoking is a modern health hazard, and it is preventable. It starts in adolescence for 90% of adults with an average age of onset ranging between 13 - 15 years and is commoner among males. This study is aimed at the prevalence, pattern, and factors affecting Cigarette smoking among undergraduate students in a tertiary institution in Plateau State. Method: A cross-sectional descriptive study involving 290 undergraduate students of the University of Jos was selected using the multistage sampling method. Results: The prevalence of cigarette use was 5.3%. Seven (70.0%) of students smoke daily, 6 (60.0%), smoke cigarettes before Lecture Hours, and 90.0% are unwilling to stop smoking. Smoking was done to experience the highness feeling, 8 (80.0%), peer smoking 8 (80.0%), to reduce stress and tension 5 (50.0%), and Smoking for Fun 7 (70.0%). Most students first smoked a cigarette when with friends 6 (60.0%). Factors significantly associated with the current use of cigarettes among the respondents were religion (χ2 = 4.167, p = 0.041) Level/year of study (χ2 = 32.266, p ≤ 0.001), and type of family (χ2 = 6.271, p = 0.043). Conclusion: Most students smoke daily, smoke before lectures start, and are unwilling to stop smoking. Health-promotion program to help smoking cessation and prevent initiation of smoking is recommended.

Cigarette induced release of exo-miR-34a from 16HBE vesicles targeting CASP2 promoted the proliferation of COPD MRC-5 cell

Objective:To explore how cigarette smoke extract(CES)regulates the expression of exosomal miR-34a in 16 HBE bronchial epithelial cells,thus affecting the proliferation of MRC-5 lung fibroblasts.Methods:CES was prepared from commercially available cigarettes,and 16HBE cells were treated with CES.The exosomal miR-34a collected from Yipeng Ding,Chief Physician,M.D..the supernatant was used for MRC-5 cell culture.The expression level of exosomal miR-34a was detected by RT-PCR.The proliferation ability of MRC-5 cells was determined by CCK-8 cell counting kit.The expression of CASP2 was detected by Western blot,and the target binding of miR-34a and CASP2 gene was verified by dual luciferase.Results:Under the transmission electron microscope,the exosomes in the supernatant of 16 HBE were spherical,with a particle size of about 100 nm;after CES treatment,the expression of exosomal miR-34a significantly increased.Further research showed that the exosomal miR-34a induced by CES can promote the proliferation of MRC-5 cells;miR-34a and CASP2 have a target binding relationship;miR-34a mimic significantly inhibited the expression of CASP2.Conclusion:In CES-induced 16HBE cells,exosomal miR-34a plays a key role in fibroblast proliferation through target binding with the CASP2 gene.

Evidence relating cigarette,cigar and pipe smoking to lung cancer and chronic obstructive pulmonary disease:Meta-analysis of recent data from three regions

BACKGROUND There is a need to have up-to-date information for various diseases on the risk related to the use of different smoked products and the use of other nicotinecontaining products.Here,we contribute to the information pool by presenting up-to-date quantitative evidence for North America,Europe and Japan and for both lung cancer and chronic obstructive pulmonary disease(COPD)on the relative risk(RR)relating to current vs never product use for each of the three smoked tobacco products,cigarettes,cigars and pipes.AIM To estimate lung cancer and COPD current smoking RRs for the three products using recent data for the three regions.METHODS Publications in English from 2010 to 2020 were considered that,based on epidemiological studies in the three regions,estimated the current smoking RR of lung cancer and/or COPD for one or more of the three products.The studies should involve at least 100 cases of the disease considered,not be restricted to specific lung cancer types or populations with specific medical conditions,and should be of cohort or nested case-control study design or randomized controlled trials.Literature searches were conducted on MEDLINE separately for lung cancer and for COPD,examining titles and abstracts initially,and then full texts.Additional papers were sought from reference lists of selected papers,reviews and metaanalyses.For each study identified,the most recent available data on each product were entered on current smoking,as well as on characteristics of the study and the RR estimates.Combined RR estimates were derived using random-effects meta-analysis.For cigarette smoking,where far more data were available,heterogeneity was studied by a wide range of factors.For cigar and pipe smoking,a more limited heterogeneity analysis was carried out.Results were compared with those from previous meta-analyses published since 2000.RESULTS Current cigarette smoking:For lung cancer,44 studies(26 North American,14 European,three Japanese,and one in multiple continents),gave an overall estimate of 12.14[95%confidence interval(CI)10.30-14.30].The estimates were higher(heterogeneity P<0.001)for North American(15.15,CI 12.77-17.96)and European studies(12.30,CI 9.77-15.49)than for Japanese studies(3.61,CI 2.87-4.55),consistent with previous evidence of lower RRs for Asia.RRs were higher(P<0.05)for death(14.85,CI 11.99-18.38)than diagnosis(10.82,CI 8.61-13.60).There was some variation(P<0.05)by study population,with higher RRs for international and regional studies than for national studies and studies of specific populations.RRs were higher in males,as previously reported,the within-study male/female ratio of RRs being 1.52(CI 1.20-1.92).RRs did not vary significantly(P≥0.05)by other factors.For COPD,RR estimates were provided by 18 studies(10 North American,seven European,and one Japanese).The overall estimate of 9.19(CI 6.97-12.13),was based on heterogeneous data(P<0.001),and higher than reported earlier.There was no(P>0.1)variation by sex,region or exclusive use,but limited evidence(0.05<P<0.1)that RR estimates were greater where cases occurring shortly after baseline were ignored;where bronchiectasis was excluded from the COPD definition;and with greater confounder adjustment.Within-study comparisons showed adjusted RRs exceeded unadjusted RRs.Current cigar smoking:Three studies gave an overall lung cancer RR of 2.73(CI 2.36-3.15),with no heterogeneity,lower than the 4.67(CI 3.49-6.25)reported in an earlier review.Only one study gave COPD results,the RR(2.44,CI 0.98-6.05)being imprecise.Current pipe smoking:Four studies gave an overall lung cancer RR of 4.93(CI 1.97-12.32),close to the 5.20(CI 3.50-7.73)given earlier.However,the estimates were heterogeneous,with two above 10,and two below 3.Only one study gave COPD results,the RR(1.12,CI 0.29-4.40),being imprecise.For both diseases,the lower RR estimates for cigars and for pipes than for current smoking of cigarettes aligns with earlier published evidence.CONCLUSION Current cigarette smoking substantially increases lung cancer and COPD risk,more so in North America and Europe than Japan.Limited evidence confirms lower risks for cigars and pipes than cigarettes.

Evidence relating cigarettes,cigars and pipes to cardiovascular disease and stroke:Meta-analysis of recent data from three regions

BACKGROUND More recent data are required relating to disease risk for use of various smoked products and of other products containing nicotine.Earlier we published metaanalyses of recent results for chronic obstructive pulmonary disease and lung cancer on the relative risk(RR)of current compared to never product use for cigarettes,cigars and pipes based on evidence from North America,Europe and Japan.We now report corresponding up-to-date evidence for acute myocardial infarction(AMI),ischaemic heart disease(IHD)and stroke.AIM To estimate,using recent data,AMI,IHD and stroke RRs by region for current smoking of cigarettes,cigars and pipes.METHODS Publications in English from 2015 to 2020 were considered that,based on epidemiological studies in the three regions,estimated the current smoking RR of AMI,IHD or stroke for one or more of the three products.The studies should involve at least 100 cases of stroke or cardiovascular disease(CVD),not be restricted to populations with specific medical conditions,and should be of cohort or nested case-control study design or randomized controlled trials.A literature search was conducted on MEDLINE,examining titles and abstracts initially,and then full texts.Additional papers were sought from reference lists of selected papers,reviews and meta-analyses.For each study identified,we entered the most recent available data on current smoking of each product,as well as the characteristics of the study and the RR estimates.Combined RR estimates were derived using random-effects meta-analysis for stroke and,in the case of CVD,separately for IHD and AMI.For cigarette smoking,where far more data were available,heterogeneity was studied by a wide range of factors.For cigar and pipe smoking,a more limited heterogeneity analysis was carried out.A more limited assessment of variation in risk by daily number of cigarettes smoked was also conducted.RESULTS Current cigarette smoking:Ten studies gave a random-effects RR for AMI of 2.72[95%confidence interval(CI):2.40-3.08],derived from 13 estimates between 1.47 and 4.72.Twenty-three studies gave an IHD RR of 2.01(95%CI:1.84-2.21),using 28 estimates between 0.81 and 4.30.Thirty-one studies gave a stroke RR of 1.62(95%CI:1.48-1.77),using 37 estimates from 0.66 to 2.91.Though heterogeneous,only two of the overall 78 RRs were below 1.0,71 significantly(P<0.05)exceeding 1.0.The heterogeneity was only partly explicable by the factors studied.Estimates were generally higher for females and for later-starting studies.They were significantly higher for North America than Europe for AMI,but not the other diseases.For stroke,the only endpoint with multiple Japanese studies,RRs were lower there than for Western studies.Adjustment for multiple factors tended to increase RRs.Our RR estimates and the variations by sex and region are consistent with earlier meta-analyses.RRs generally increased with amount smoked.Current cigar and pipe smoking:No AMI data were available.One North American study reported reduced IHD risk for non-exclusive cigar or pipe smoking,but considered few cases.Two North American studies found no increased stroke risk with exclusive cigar smoking,one reporting reduced risk for exclusive pipe smoking(RR 0.24,95%CI:0.06-0.91).The cigar results agree with an earlier review showing no clear risk increase for IHD or stroke.CONCLUSION Current cigarette smoking increases risk of AMI,IHD and stroke,RRs being 2.72,2.01 and 1.62.The stroke risk is lower in Japan,no increase was seen for cigars/pipes.

Stubbing Out the Cigarette

China has rolled out laws,policies,and programs to reduce the use of tobacco,and achieved marked results over the past decades.OLD Chen took a drag on his cigarette,watching his three-year-old granddaughter woddle around in a small park in western Beijing.Whenever the toddler came near,he would stretch out his hand holding the cigarette as far away from her as possible.Still,the smell of smoke was perceptible even at arm’s length.“Smoking is no good,my wife complains about it every day,”he acknowledged.“But I am too old to quit,”he said,giving a familiar excuse.Like many men of his generation,the 67-year-old first picked up the nicotine habit from his peers,fellow factory workers in his case.He has noticed that fewer people of his age are smoking today.“Smoking is no good,”he reiterated.

Analysis on the Development of Cigarette Packaging in the Era of Intelligence

China is one of the biggest countries in cigarette production and sales,therefore it is important to improve the quality and efficiency of cigarette production.As cigarette packaging is an important part in cigarette production,therefore,it is important to strengthen research on improving the quality of cigarette packaging.This article summarizes the development process of cigarette packaging in China,introduces the development of printing technology in the era of intelligence,summarizes the application of printing technology in cigarette packaging,analyzes and explores the development trend of cigarette packaging in the era of intelligence,with the hope to provide reference for practitioners.

Immediate Respiratory Response to Electronic Cigarette Use

Background: Electronic cigarettes were originally designed to reduce adult dependency on normal cigarettes and as a tobacco cessation tool to substitute traditional cigarettes. But it has become the most popular among teenagers. Rationale: To investigate the immediate adverse respiratory effect of short-term electronic cigarette vapor inhalation. Method: Twenty-five subjects were randomly selected and used in this study. The respiratory resistance values were evaluated and used for comparison. The subjects were asked to breathe into the Airflow Perturbation Device (APD) for evaluation of their respiratory resistance before vaping (in triplicate). The same subjects, a minute later, were then asked to use one poke (3 seconds) of the e-Cigarette device to inhale e-Cigarette vapor with nicotine from a pod with 59 mg/ml nicotine. Immediately following the e-Cigarette use, their respiratory resistance was measured again (in triplicate). Results: Comparing the respiratory resistance values before and immediately after exposure to e-Cigarette vapor showed that their respiratory resistance increased almost immediately. Conclusion: Although there are long-term studies showing that the e-Cigarette is as harmful as regular cigarettes, this study showed a nearly immediate effect of using the e-Cigarette that significantly increased the respiratory resistance of the user. Very short exposure time to e-Cigarette vapor (3 seconds only), caused an immediate adverse physiologic effect in respiratory resistance.

Prophylactic Anti-inflammation Inhibits Cigarette Smoke-induced Emphysema in Guinea Pigs

In this study, the effect of prophylactic anti inflammation on the development of smoke induced emphysema was investigated. Young male guinea pigs aged 1.5 - 2 months (weighing 198.3±26.9 g) were randomly divided into 4 groups: group A (cigarette smoke exposure only), group B (cigarette smoke exposure plus pentoxifylline rich (PTX, 10 mg/d) forage feeding), group C (cigarette smoke exposure plus intermittent cortical steroid injection (Triamcinolone acetonide, 3 mg, im, every three weeks) and control group (group D: animals with sham smoke exposure, raised under the same conditions). Animals in group A, B and C were exposed to smoke of cigarettes for 1 to 1.5 h twice a day, 5 days a week. All animals were killed at the 16th week and followed by morphometrical analysis of the midsagittal sectioned lung slices. Smoke exposure of 16 weeks resulted in visible emphysematous development in Group A but not in Group B and C. It was evidenced by the indicator of air space size, mean linear intercept (L m): 120.6±16.0 μm in Group A; 89.8±9.2 μm in Group B and 102.4±17.7 μm in Group C. The average L m in either group B or group C was shorter than that in Group A (ANOVA and Newman Keuls test, F=8.80, P =0.0002) but comparable to that (94.8±13.2 μm) in group D ( P >0.05). It is concluded that long term prophylactic anti inflammation inhibits pulmonary emphysema induced by cigarette smoking in the guinea pigs.

Research on cigarette during smoking based on reverse engineering and numerical simulation

The three-dimensional(3 D)model of cigarette was accurately constructed through reverse engineering as the research object of numerical simulation.The combustion process of cigarette was studied with computational fluid dynamics(CFD).Standard Laminar models with species transport approach were applied,and numerical simulation of the cigarette was analyzed with semi-implicit method for pressure–velocity coupling.The results showed that the model could predict velocity of cigarette smoke,the distributions of temperature and pressure at different times.In order to verify the correctness of model,it was found that the relationship between the velocity of smoke and pressure according to Darcy’s law on z position(x=4 mm,y=0,0 mm≤z≤50.61 mm).

Cigarette smoking and alcohol drinking and esophageal cancer risk in Taiwan Residents women

AIM:To investigate the etiology of esophageal cancer among Taiwan Residents women.METHODS:This is a multi-center,hospital-based,case-control study.Case patients consisted of women who were newly diagnosed and pathology-proven to have esophageal squamous cell carcinoma(ESCC) from three large medical centers(one from Northern and two from Southern Taiwan,respectively)between August 2000 and December 2008.Each ESCC patient was matched with 4 healthy women based on age(within 3 years)and hospital of origin,from the Department of Preventive Medicine in each hospital.A total of 51 case patients and 204 controls,all women,were studied.RESULTS:Frequencies of smokers and drinkers among ESCC patients were 19.6%and 21.6%,respectively,which were significantly higher than smokers(4.4%) and drinkers(4.4%)among controls(OR=4.07,95%CI:1.36-12.16,P=0.01;OR=3.55,95%CI:1.03-12.27,P=0.04).Women who drank an amount of alcohol more than 158 g per week had a 20.58-fold greater risk(95%CI:1.72-245.62,P=0.02)of ESCC than those who never drank alcohol after adjusting for other covariates,although the sample size was small.CONCLUSION:Cigarette smoking and alcohol drinking,especially heavy drinking,are the major risks for developing ESCC in Taiwan Residents women.

Vascular and Morphogenetic Abnormalities Associated with Exposure of Cigarette Smoke Condensate during Chicken and Murine Embryogenesis

Objective Embryonic movements （EM） and angiogenesis pathways are evolutionarily conserved mechanisms which are essential for proper embryonic development. Deviations in these processes by exposure to cigarette smoke condensate （CSC） may cause vascular and morphogenetic disorders. Methods Using chicken and mouse embryos, we have demonstrated the in vivo effects of CSC on EM, vascular development, and organogenesis. Results Examination of the CSC exposed chicken embryos revealed a significant reduction in EM, stunted growth, deviated pattern of blood vessels, hemorrhages, and localized necrosis. Likewise, mouse embryos that were exposed to CSC at E8.5 and E9.5 died between E11.5 and E12.5, respectively. These mouse embryos showed defects in morphogenesis and remodeling of the embryonic vasculature, while littermate controls showed normal development. Conclusion Cigarette smoking during pregnancy is fatal for growing embryos. CSC may induce the remodeling of embryonic vasculature, leading to various pathologies.

Effects of Puerarin on Pulmonary Vascular Remodeling and Protein Kinase C-α in Chronic Cigarette Smoke Exposure Smoke-exposed Rats

In order to investigate the effects of puerarin on pulmonary vascular remodeling and protein kinase C-α （PKC-α） in chronic exposure smoke rats, 54 male Wistar rats were randomly divided into 7 groups： control group （C group）, smoke exposure groups （S4w group, S8w group）, puerarin groups （P4w group, P8w group）, propylene glycol control groups （PC4w group, PC8w group）. Rats were exposed to cigarette smoke or air for 4 to 8 weeks. Rats in puerarin groups also received puerarin. To evaluate vascular remodeling, alpha-smooth muscle actin （α-SM-actin） staining was used to count the percentage of completely muscularised vessels to intraacinar pulmonary arteries （CMA/IAPA） which was determined by morphometric analysis of histological sections. Pulmonary artery smooth muscle cell （PASMC） apoptosis was detected by in situ end labeling technique （TUNEL）, and proliferation by proliferating cell nuclear antigen （PCNA） staining. Reverse transcription-polymerase chain reaction （RT-PCR）, immunofluorescence staining and Western blot analysis were done to detect the PKC-α mRNA and protein expression in pulmonary arteries. The results showed that in cigarette smoke-exposed rats the percentage of CMA/IAPA and α-SM-actin expression were increased greatly, PASMC apoptosis was increased and proliferation was markedly increased; Apoptosis indices （AI） and proliferation indices （PI） were higher than in C group; AI and PI were correlated with vascular remodeling indices; The expression of PKC-α mRNA and protein in pulmonary arteries was significantly higher than in C group. In rats treated with puerarin, the percentage of CMA/IAPA and cell proliferation was reduced, whereas PASMC apoptosis was increased; The expression levels of PKC-α mRNA and protein were lower than in smoke exposure rats. There was no difference among all these data between S groups and PC groups. These findings suggested that cigarette smoke-induced pulmonary vascular remodeling was most likely an effect of the imbalance of PASMC proliferation and apoptosis. Puerarin appears to be able to reduce cell proliferation and vascular remodeling possibly through PKC signaling transduction pathway.

Effect of Cigarette Smoke Extract on the Role of Protein Kinase C in the Proliferation of Passively Sensitized Human Airway Smooth Muscle Cells

To investigate the effect of cigarette smoke extract (CSE) on the role of protein kinase C (PKC) in the proliferation of passively sensitized human airway smooth muscle cells (HASMCs). After synchronization of cultured HASMCs, they were divided into a group A and Group B. The group A was treated with normal human serum and served as controls and the group B was treated with the serum of asthma patients. The group A was further divided into group of A_1, A_2 and A_3 and the group B was sub-divided into the group of B_1, B_2, B_3, B_4 and B_5. No other agents were added to the group A_1 and B_1. The cells of group A_2 and B_2 were stimulated with 5 % CSE for 24 h. HASMCs from group A_3 and B_3 were treated with PKC agonist PMA (10 nmol/L) and CSE (5 %) for 24 h. PKC inhibitor Ro-31-8220 (5 μmol/L) was added to the HASMCs of group B_4 for 24 h. The cells from group B_5 were stimulated with Ro-31-8220 (5 μmol/L) and CSE (5 %) for 24 h. The proliferation of HASMCs isolated from group A and B was examined by cell cycle analysis, MTT colorimetric assay and 3H-TdR incorporation test. The expression of PKC-α in each group was observed by Western blotting and RT-PCR, respectively. The results showed that the percentage of S phase, absorbance (A) value, the rate of 3H-TdR incorporation, the ratios of A value of PKC-α mRNA and the A value of PKC-α protein in HASMCs from group B_1, B_2 and B_3 were significantly increased compared to those of group A_1, A_2 and A_3 correspondingly and respectively (P<0.01). The proliferation of HASMCs of group A_2 and B_2 stimulated with CSE and group A_3 and B_3 stimulated with CSE and PMA were also significantly enhanced when group A_1, A_2 and A_3 and group B_1, B_2 and B_3 compared to each other (P<0.05, P<0.01, respectively). The percentage of S phase, absorbency (A) value, 3H-TdR incorporation rate, the ratios of A value of PKC-α mRNA and the A value of PKC-α protein in HASMCs from group B_4 treated with Ro-31-8220 and group B_5 treated with CSE and Ro-31-8220 were significantly decreased as compared to those of group B_1 and B_2 correspondingly and respectively (P<0.05, P<0.01). It was concluded that CSE can enhance the passively sensitized HASMC proliferation and the expression of PKC alpha. PKC and its alpha subtype may contribute to this process. Our results suggest cigarette may play an important role in ASMCs proliferation of asthma through PKC signal pathway.

Berberine Attenuates Cigarette Smoke Extract-induced Airway Inflammation in Mice:Involvement of TGF-β1/Smads Signaling Pathway

Although several studies confirmed that berberine may attenuate airway inflammation in mice with chronic obstructive pulmonary disease(COPD),its underlying mechanisms were not clear until now.We aimed to establish an experiment mouse model for COPD and to investigate the effects of berberine on airway inflammation and its possible mechanism in COPD model mice induced by cigarette smoke extract(CSE).Twenty SPF C57BL/6 mice were randomly divided into PBS control group,COPD model group,low-dose berberine group and high-dose berberine group,5 mice in each group.The neutrophils and macrophages were examined by Wright's staining.The levels of inflammatory cytokines TNF-α and IL-6 in bronchoalveolar lavage fluid(BALF)were detennined by enzyme-linked immunosorbent assay.The expression levels of TGF-β1,Smad2 and Smad3 mRNA and proteins in lung tissues were respectively detected by quantitative real-time polymerase chain reaction and Western blotting.It was found that CSE increased the number of inflammation cells in BALF,elevated lung inflammation scores,and enhanced the TGF-β1/Smads signaling activity in mice.High-dose berberine restrained the alterations in the COPD mice induced by CSE.It was concluded that high-dose berberine ameliorated CSE-induced airway inflammation in COPD mice.TGF-β1/Smads signaling pathway might be involved in the mechanism.These findings suggested a therapeutic potential of high-dose berberine on the CSE-induced airway inflammation.

Injury of Mouse Brain Mitochondria Induced by Cigarette Smoke Extract and Effect of Vitamin C on It in vitro

Objective To investigate the toxicity of cigarette smoke extract (CSE) and nicotine on mouse brain mitochondria as well as the protective effect of vitamin C in vitro. Method Mouse brain mitochondria in vitro was incubated with CSE or nicotine in the absence or presence of vitamin C for 60 minutes, and the changes of mitochondrial function and structure were measured. Results CSE inhibited mitochondrial ATPase and cytochrome C oxidase activities in a dose-dependent manner. However, no significant changes in the peroxidation indices were observed when mitochondrial respiratory enzymes activity was inhibited, and protection of mitochondria from CSE-induced injury by vitamin C was not displayed in vitro. The effect of CSE on mouse brain mitochondria swelling response to calcium stimulation was dependent on calcium concentrations. CSE inhibited swelling of mitochondria at 6.5μmol/L Ca2+, but promoted swelling response at 250μmol/L Ca2+. Nicotine, the major component of cigarette smoke, showed no significant damage in mouse brain mitochondria in vitro. The CSE treatment induced mitochondrial inner membrane damage and vacuolization of the matrix, whereas the outer mitochondrial membrane appeared to be preserved. Conclusion The toxic effect of CSE on brain mitochondria may be due to its direct action on enzymatic activity rather than through oxygen free radical injury. Nicotine is not the responsible component for the toxicity of CSE to brain mitochondria.

Exercise Training Attenuated Chronic Cigarette Smoking-induced Up-regulation of FIZZ1/RELMα in Lung of Rats

FIZZ/RELM is a new gene family named ＂found in inflammatory zone＂ （FIZZ） or ＂re- sistin-like molecule＂ （RELM）. FIZZ1/RELMct is specifically expressed in lung tissue and associated with pulmonary inflammation. Chronic cigarette smoking up-regulates FIZZ 1/RELMct expression in rat lung tissues, the mechanism of which is related to cigarette smoking-induced airway hyperresponsive- ness. To investigate the effect of exercise training on chronic cigarette smoking-induced airway hyper- responsiveness and up-regulation of FIZZ1/RELMct, rat chronic cigarette smoking model was estab- lished. The rats were treated with regular exercise training and their airway responsiveness was meas- ured. Hematoxylin and eosin （HE） staining, immunohistochemistry and in situ hybridization of lung tissues were performed to detect the expression of FIZZ1/RELMct. Results revealed that proper exercise training decreased airway hyperresponsiveness and pulmonary inflammation in rat chronic cigarette smoking model. Cigarette smoking increased the mRNA and protein levels of FIZZ1/RELMct, which were reversed by the proper exercise. It is concluded that proper exercise training prevents up-regulation of FIZZ1/RELMct induced by cigarette smoking, which may be involved in the mechanism of proper exercise training modulating airway hyperresponsiveness.

Roles of TGF-β Signaling Pathway in Endoplasmic Reticulum Stress in Endothelial Cells Stimulated with Cigarette Smoke Extract

To investigate the role of signaling pathway in the effect of endoplasmic reticulum stress（ER stress） in endothelial cells stimulated with cigarette smoke extract（CSE）. Human umbilical vein endothelial cells（HUVECs） were cultured and divided into 3 groups： CSE-stimulated group, CSE-stimulated with 4-PBA group, and negative control group. HUVECs were cultured and stimulated with CSE at concentrations of 5%, 10% and 20%, respectively, mR NA of CXCL-8 and GRP78 was detected by real-time PCR. ELISA was performed to test the expression of CXCL-8 protein, and neutrophils migration was detected by Transwell board test. The NF-κB, ERK, p38 MAPK and transforming growth factor beta（TGF-β） were detected by flow cytometry. The mRNA of CXCL-8 and GRP78 increased in CSE-stimulated HUVECs（P〈0.05）. Furthermore, it was concentration-dependent. 4-PBA significantly reduced the expression of CXCL-8 protein（P〈0.05） and neutrophil migration（P〈0.05）. The TGF-β, rather than the NF-κB, ERK and P38 MAPK pathway might be involved in ER stress stimulated by CSE. CSE induced neutrophils migration by increasing the expression of CXCL-8 in endothelial cells. ER stress might play a role in the effect of neutrophils migration stimulated with CSE, and TGF-β pathway may contribute to the ER stress in HUVECs.

Cigarette Smoke Extract Inhibits the Proliferation of Alveolar Epithelial Cells and Augments the Expression of P21^(WAF1)

Cigarette smoking is intimately related with the development of chronic obstructive pulmonary diseases, and alveolar epithelium is a major target for the exposure of cigarette smoke extract. In order to investigate the effect of cigarette smoke extract on the proliferation of alveolar epithelial cell type Ⅱ and its relationship with P21^WAF1, the alveolar epithelial type Ⅱ cell line （A549） cells were chosen as surrogate cells to represent alveolar epithelial type Ⅱ cells. MTT assay was used to detect cell viability after interfered with different concentrations of cigarette smoke extract. It was observed cigarette smoke extract inhibited the growth of A549 cells in a dose- and time-dependent manner. The morphological changes, involving the condensation and margination of nuclear chromatin, even karyorrhexis, were observed by both Hoechst staining and electronic microscopy. Flow cytometry analysis demonstrated the increased cell percentages in G1 and subG1 phases after the cells were incubated with cigarette smoke extract. The expression of p21^WAF1 protein and mRNA was also significantly increased as detected by the methods of Western blot or reverse transcription-polymerase chain reaction respectively. In conclusion, cigarette smoke extract inhibits the proliferation of alveolar epithelial cell type Ⅱ and blocks them in G1/S phase. The intracelhilar accumulation of P21^WAF1 may be one of the mechanisms which contribute to cigarette smoke extract-induced inhibition of cell proliferation.