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cigarette smoke‑induced malignant transformation via STAT3 signalling in pulmonary epithelial cells in a lung‑on‑a‑chip model

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Bio-Design and Manufacturing 2020年第4期3卷 383-395页

作者： Wei Hou Siyi Hu Ken‑tye Yong Jie Zhang Hanbin Ma CAS Key Laboratory of Bio‑Medical Diagnostics Suzhou Institute of Biomedical Engineering and TechnologyChinese Academy of SciencesNo.88 Keling RoadHuqiu DistrictSuzhou 215163JiangsuPeople’s Republic of China Department of Respiratory and Critical Care Medicine The Second Hospital of Jilin UniversityNo.218 Ziqiang StreetNanguan DistrictChangchun 130041JilinPeople’s Republic of China School of Electrical and Electronic Engineering Nanyang Technological UniversitySingapore 639798Singapore

Background Chronic obstructive pulmonary disease(COPD)is a severe public health *** smoke(CS)is a risk factor for COPD and lung *** underlying molecular mechanisms of CS-induced malignant transformation of bronchial epithelial cells remain *** this study,we describe a lung-on-a-chip to explore the possible mechanistic link between cigarette smoke extract(CSE)-associated COPD and lung *** An in vitro lung-on-a-chip model was used to simulate pulmonary epithelial cells and vascular endothelial cells with *** levels of IL-6 and TNF-αwere tested as indicators of inflammation using an enzyme-linked immune sorbent *** junction complex mRNA expression was detected with qRT-PCR as the index of epithelial-to-mesenchymal transition(EMT).The effects of CSE on the phosphorylation of signal transduction and transcriptional activator 3(STAT3)were detected by Western *** cytometry was performed to investigate the effects of this proto-oncogene on cell cycle *** Inflammation caused by CSE was achieved in a lung-on-a-chip model with a mimetic *** exposure induced the degradation of intercellular connections and triggered the EMT *** exposure also activated the phosphorylation of proto-oncogene STAT3,while these effects were inhibited with *** CSE exposure in the lung-on-a-chip model caused activation of STAT3 in epithelial cells and endothelial ***0152,an inhibitor of activated STAT3,could be a potential treatment for CS-associated COPD and lung cancer.

关键词： cigarette smoke Microfluidic chips STAT3 Chronic obstructive pulmonary disease

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

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2008年第1期28卷 27-32页

作者：朱朝霞徐永健邹晖张珍祥倪望陈士新 Department of Respiratory Medicine Tongji Hospital Tongji Medical College Huazhong University of Science and Technology

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

关键词： puerarin vessel remodeling cigarette smoke protein kinase C apoptosis proliferation

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Prophylactic Anti-inflammation Inhibits cigarette smoke-induced Emphysema in Guinea Pigs

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2003年第4期23卷 365-368页

作者：张劲农陶晓南谢建敏向敏付薇 Department of Respiratory Diseases

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.

关键词： cigarette smoke pulmonary emphysema prophylactic anti inflammation

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The Differential Effects of Chronic Alcohol and cigarette smoke Exposures on Cognitive-Behavioral Dysfunction in Long Evans Rats

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Journal of Behavioral and Brain Science 2022年第9期12卷 413-432页

作者： Emine B. Yalcin Büşra Nur Delikkaya William Pelit Ming Tong Suzanne M. De La Monte Sharon Rounds Division of Research Providence VA Medical Center Providence RI USA Liver Research Center Division of Gastroenterology and Department of Medicine Rhode Island Hospital and the Alpert Medical School of Brown University Providence RI USA Chemical Biology and English Brown University Providence RI USA Departments of Medicine Neurology and Pathology and Laboratory Medicine Rhode Island Hospital Women & Infants Hospital of Rhode Island Alpert Medical School of Brown University Providence VA Medical Center Providence RI USA Departments of Medicine and Pathology and Laboratory Medicine Warren Alpert Medical School of Brown University Vascular Research Laboratory Providence VA Medical Center Providence RI USA

Background and Objective: Chronic heavy alcohol consumption and daily cigarette smoking are the most prevalent substance use problems in the U.S., including Veterans. Excessive alcohol use causes neurocognitive and behavioral deficits that can be linked to neurodegeneration. Similarly, preclinical and clinical data suggest that smoking also leads to brain atrophy. This study examines the differential and additive effects of alcohol and cigarette smoke (CS) exposures on cognitive-behavioral function. Methods: A 4-way experimental model of chronic alcohol and CS exposures was generated using 4-week-old male and female Long Evans rats that were pair-fed with Lieber-deCarli isocaloric liquid diets containing 0% or 24% ethanol for 9 weeks. Half of the rats in the control and ethanol groups were exposed to CS for 4 hours/day and 4 days/week for 9 weeks. All rats were subjected to Morris Water Maze, Open Field, and Novel Object Recognition testing in the last experimental week. Results: Chronic alcohol exposure impaired spatial learning as shown by significantly increased latency to locate the platform, and it caused anxiety-like behavior marked by the significantly reduced percentage of entries to the center of the arena. Chronic CS exposure impaired recognition memory as suggested by significantly less time spent at the novel object. Combined exposures to alcohol and CS did not show any significant additive or interactive effect on cognitive-behavioral function. Conclusion: Chronic alcohol exposure was the main driver of spatial learning, while the effect of secondhand CS exposure was not robust. Future studies need to mimic direct CS exposure effects in humans.

关键词： Alcohol cigarette smoke Spatial Learning Recognition Memory Anxiety White Matter Rat

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N-acetylcyteine and flavonoid rich diet:The protective effect of 15 different antioxidants on cigarette smoke-damaged primary human osteoblasts

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Advances in Bioscience and Biotechnology 2012年第8期3卷 1129-1139页

作者： Sabrina Ehnert Stefan Dobele Karl Friedrich Braun Britta Burkhardt Valeska Hofmann Mario Hausmann Jose Tomas Egana Ulrich Stockle Thomas Freude Andreas Klaus Nussler Department of Traumatology Eberhard Karls Universitat TübingenTübingenGermany Department of Traumatology MRITechnische Universitat MünchenMünchenGermany Department of Plastic Surgery and Hand Surgery Technische Universitat MünchenMünchenGermany FONDAP Center for Genome Regulation Facultad de CienciasUniversidad de ChileSantiagoChile

cigarette consumption increases oxidative stress in many organs. Increased oxidative stress harms bone cells, which negatively affects bone-matter and -stability. This leads to an increased fracture risk and delayed fracture healing in smokers. A supporting therapy with antioxidants could be of great benefit for surgeons dealing with delayed fracture healing due to increased oxidative stress. In this article we complement and compare our published data with hitherto unpublished data and show the protective effect of 15 different antioxidants on cigarette smoke induced damage in primary human osteoblasts. Exposure to cigarette smoke medium (CSM) rapidly induces formation of ROS in osteoblasts in a concentration- and time-dependent manner. Massive cell damage is seen already after 4 h (EC50 ≈ 0.75 OD320). Pre-, co- and post-incubation with the different antioxidants reduces the formation of ROS and consequently improves the viability of the CSM exposed osteoblasts. Small compounds, e.g. N-acetylcysteine, proved highly effective if pre- or co-incubated before exposure to the CSM. Thus, they are good candidates for acute therapy support as they can be administered in high doses. However, our data suggest that a balanced daily diet could lead to an accumulation of various natural antioxidants (flavonoids) that effectively protect osteoblasts from oxidative stress-induced damage in all three settings investigated. Together with their partly phytoestrogenic properties this may even abate alterations in bone and thus reduce fracture risk on the long run.

关键词： cigarette smoke Osteoblasts Oxidative Stress N-Acetylcysteine Flavonoids

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Unveiling the dynamic role of innate and adaptive immune cells in COPD pathogenesis induced by cigarette smoke

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Life Research 2024年第4期7卷 29-41页

作者： Dur E Maknoon Razia Syed Sib Tul Hassan Shah Tabish Faheem Department of Pathogen Biology College of Basic Medical SciencesJilin UniversityChangchun 130015China Zhejiang Province Key Laboratory of Plant Secondary Metabolism and Regulation College of Life Sciences and MedicineZhejiang Sci-Tech UniversityHangzhou 310018China Department of Surgery Nishtar Medical universityMultan 66000Pakistan.

Chronic obstructive pulmonary disease(COPD)is a multifaceted syndrome characterized by a dysregulated inflammatory cascade within the respiratory system,primarily triggered by exposure to harmful particles and gases,notably from cigarette *** inflammatory response is orchestrated by innate immune cells like macrophages and epithelial cells,which recognize danger signals released from damaged *** inflammation prompts an adaptive immune reaction mediated by dendritic cells,culminating in the formation of lymphoid follicles and involving a complex interplay of T and B cells,as well as cytotoxic ***,both viral and bacterial infections exacerbate COPD by further igniting inflammatory pathways,perpetuating the chronic inflammatory *** comprehensive review encapsulates the intricate interplay between innate and adaptive immunity in COPD,with a particular focus on the role of cigarette smoke in its pathogenesis and potential therapeutic targets.

关键词： chronic obstructive pulmonary disease innate immunity adaptive immunity cigarette smoke inflammation oxidative stress protease-antiprotease imbalance

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Lyn mediates cigarette smoke Extract(CSE)-induced Cellular Cytotoxicity

Lyn mediates Cigarette Smoke Extract(CSE)-induced Cellular C...

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细胞—生命的基础——中国细胞生物学学会2013年全国学术大会·武汉

作者： Wenxue Wang Qinghua Cui Min Wu School of Life Sciences Yunnan University Department of Biochemistry and Molecular Biology University of North DakotaGrand Forks

It is well established that cigarette smoke induces a series of lung diseases such as lung inflammation, chronic obstructive pulmonary disease(COPD),asthma,and particularly increases lung cancer risks. Lyn,a member of Src kinase family,is a critical signaling mediator regulating cell proliferation, differentiation,apoptosis,immune response and ***,It is unknown whether Lyn is

关键词： Lyn cigarette smoke Cytotoxicity Inflammation JAK2/STAT1 pathway

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The anti-apoptotic effect of hydrogen sulfide attenuates injuries to the medullary respiratory centers of neonatal rats subjected to in utero cigarette smoke exposure

The anti-apoptotic effect of hydrogen sulfide attenuates inj...

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中国生理学会张锡钧基金会第十三届全国青年优秀生理学学术论文交流及评奖会议、中国生理学会第十一届全国青年生理学工作者学术会议

作者： Lihong Nie Yajie Hu Xiang Yan Mingqiang Li Li Chen Hui Li Xianke Li Hua Zhou Yu Zheng Department of Physiology West China School of Preclinical and Forensic MedicineSichuan University Department of Physiology School of Basic Medical SciencesNingxia Medical University

Noxious substances released from burning cigarettes may cause hypoxia,ischemia and neurotoxic effects that impede the development of the central nervous system,including brainstem respiratory *** previous studies demonstrated that hydrogen sulphide（H S） could protect medullary respiratory centres from the injuries caused by hypoxia in in vitro preparations from neonatal *** present experiments were carried out to study the protective effects of H S,potentially mediated by an anti-apoptotic mechanism,against injury of the medullary respiratory centres induced by intrauterine cigarette smoke *** SD rats were divided into 4 groups,including control,cigarette smoke exposure（CS）,CS+NaHS（a donor of H S） and NaHS *** frequencies（BF） were recorded from the hypoglossal rootlets of medullary slices from the neonatal rats,and hypoxia was induced in all groups to unmask possible differential BF responses in the rootlets to *** staining was performed to examine injuries sustained by the neurons of medullary *** staining and the expression of activated caspase-3 protein were used to assay apoptosis in the medulla ***-2 and Bax protein and gene expression were analysed by western blotting and RT-PCR,*** observed that hypoxia decreased BF in CS neonatal rats and that NaHS offset hypoxia-induced respiratory *** examination after Nissl staining indicated that NaHS alleviated the injuries sustained by neurons after intrauterine cigarette smoke *** also showed that NaHS decreased the number of TUNEL-positive neurons and the expression of activated caspase-3 protein in the medulla oblongata of CS neonatal ***,NaHS promoted Bcl-2 protein expression and reduced Bax protein and mRNA expression in the medulla oblongata of CS neonatal ***,the present study indicated that H S protects medullary respiratory centres against the insult induced by intrauterine cigarette smo

关键词： hydrogen sulfide cigarette smoke tobacco apoptosis medullary respiratory centre neonatal rat

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Modifying NaY Zeolite with Metal Oxide by Microwave Irradiation:Influence on the Adsorption and Decomposition of N-nitrosamines

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Chinese Chemical Letters 2000年第7期11卷 649-652页

作者： Li Li MA Bin SHEN Jian Hua ZHU Jia Rong XIA Qin Hua XU(Chemistry Department, Nanjing University, Nanjing 210093) Chemistry Department Nanjing University Nanjing 210093 China

Coating *** ZrO2 on zeolite NaY accelerated decomposition of N-nitrosodimethylamine and N-nitrosopyrrolidine, resulting from variation of the surface state such as generation of basic sites.

关键词： zeolite NaY MgO ZrO2 N-nitrosamines cigarette smoke

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Assessment of tobacco heating system 2.4 on osteogenic differentiation of mesenchymal stem cells and primary human osteoblasts compared to conventional cigarettes

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World Journal of Stem Cells 2020年第8期12卷 841-856页

作者： Romina H Aspera-Werz Sabrina Ehnert Monja Müller Sheng Zhu Tao Chen Weidong Weng Johann Jacoby Andreas K Nussler Department of Traumatology BG Trauma ClinicSiegfried Weller Institute for Trauma ResearchEberhard Karls Universität TübingenTübingen 72076Germany Department of Traumatology BG Trauma ClinicSiegfried Weller Institute for Trauma ResearchEberhard Karls Universität TübingenTübingen 71076Germany Institute for Clinical Epidemiology and Applied Biometry Eberhard Karls Universität TübingenTübingen 71076Germany

BACKGROUND cigarette smoking(CS)is the most common method of consuming *** effects on bone integrity,increased incidence of fractures,and delayed fracture healing are all associated with *** 150 of the 6500 molecular species contained in cigarette smoke and identified as toxic compounds are inhaled by CS and,via the bloodstream,reach the skeletal *** technologies designed to develop a reduced-risk alternative for smokers are based on electronic nicotine delivery systems,such as e-cigarettes and tobacco heating systems(THS).THS are designed to heat tobacco instead of burning it,thereby reducing the levels of harmful toxic compounds *** To examine the effects of THS on osteoprogenitor cell viability and function compared to conventional *** Human immortalized mesenchymal stem cells(n=3)and primary human preosteoblasts isolated from cancellous bone samples from BG Unfall Klinik Tübingen(n=5)were osteogenically differentiated in vitro with aqueous extracts generated from either the THS 2.4“IQOS”or conventional“Marlboro”cigarettes for up to 21 *** viability was analyzed using resazurin conversion assay(mitochondrial activity)and calcein-AM staining(esterase activity).Osteogenic differentiation and bone cell function were evaluated using alkaline phosphatase(AP)activity,while matrix formation was analyzed through alizarin red *** cilia structure was examined by acetylatedα-tubulin immunofluorescent *** radical production was evaluated with 2’,7’-dichlorofluoresceindiacetate *** Our data clearly show that THS is significantly less toxic to bone cells than CS when analyzed by mitochondrial and esterase activity(Pcigarettes significantly reduced the A

关键词： Primary human osteoblast cigarette smoke Tobacco heating system Mesenchymal stem cells Electronic nicotine delivery systems Bone

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