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1.
Front Immunol ; 11: 1359, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32595653

RESUMO

SARS-CoV-2 is a new coronavirus that has caused a worldwide pandemic. It causes severe acute respiratory syndrome (COVID-19), which is fatal in many cases, and is characterized by a cytokine release syndrome (CRS). Great efforts are currently being made to block the signal transduction pathway of pro-inflammatory cytokines in order to control this "cytokine storm" and rescue severely affected patients. Consequently, possible treatments for cytokine-mediated hyperinflammation, preferably within approved safe therapies, are urgently being researched to reduce rising mortality. One approach to inhibit proinflammatory cytokine release is to activate the cholinergic anti-inflammatory pathway through nicotinic acetylcholine receptors (α7nAchR). Nicotine, an exogenous α7nAchR agonist, is clinically used in ulcerative colitis to counteract inflammation. We have found epidemiological evidence, based on recent clinical SARS-CoV-2 studies in China, that suggest that smokers are statistically less likely to be hospitalized. In conclusion, our hypothesis proposes that nicotine could constitute a novel potential CRS therapy in severe SARS-CoV-2 patients.


Assuntos
Infecções por Coronavirus/imunologia , Síndrome da Liberação de Citocina/tratamento farmacológico , Nicotina/uso terapêutico , Pneumonia Viral/imunologia , China/epidemiologia , Fumar Cigarros , Infecções por Coronavirus/tratamento farmacológico , Infecções por Coronavirus/epidemiologia , Infecções por Coronavirus/patologia , Humanos , Pandemias , Pneumonia Viral/tratamento farmacológico , Pneumonia Viral/epidemiologia , Pneumonia Viral/patologia , Índice de Gravidade de Doença , Receptor Nicotínico de Acetilcolina alfa7/agonistas
6.
J Environ Manage ; 261: 110236, 2020 May 01.
Artigo em Inglês | MEDLINE | ID: mdl-32148306

RESUMO

The fast growth in the anthropogenic activities, that involve a wide use of pharmaceuticals, has led to the appearance of new toxic and hazardous chemical compounds, called "emerging pollutants", which could cause unpredictable consequences to the ecosystems. The current review is focused on emerging pollutants occurring in food or air and include caffeine and nicotine, as well as on pharmaceuticals, in particular amoxicillin, and the concerns caused by its wide usage for medical purposes. This review, for the first time, analyzes and discusses the potential risks and implications of caffeine, nicotine and amoxicillin as emerging environmental pollutants, a field that remains underrepresented to date. Both caffeine and nicotine belong to life style compounds, while pharmaceutical amoxicillin is one of the very popular ß-lactam antibiotics used to take care of human and animal infections. The review covers the toxic effect caused by caffeine, nicotine and amoxicillin on humans and animals and describes some of the main adsorbents utilized for their removal (e.g., grape stalk, tea waste, wheat grains, bentonite, activated carbon, acid and base modified grape slurry wastes, graphene oxides, modified graphene oxides, zeolites, etc.). The isotherm and kinetic models for the analysis of caffeine, nicotine and amoxicillin adsorption by different adsorbents are presented. The impact of pH, temperature, adsorbent dosage and thermodynamic studies were deeply analyzed. The review also discusses the mechanism of adsorption for the above-mentioned emerging pollutants, which includes π-π interaction, cation-π bonding, electron-donor and electron-acceptor forces, van der Waals forces, electrostatic interactions, etc. The present review has a potential value for chemists, ecologists, toxicologists, environmental engineers, and other professionals that are involved in environmental protection.


Assuntos
Águas Residuárias , Poluentes Químicos da Água , Adsorção , Amoxicilina , Cafeína , Ecossistema , Cinética , Nicotina
7.
J Spec Oper Med ; 20(1): 37-39, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32203603

RESUMO

Atrial flutter and atrial fibrillation are among the most commonly encountered cardiac arrhythmias; however, there is a dearth of clinical trials or case studies regarding its occurrence in the setting of stimulants such as caffeine and nicotine in otherwise healthy young patients. Described here is a case of a 29-year-old physically fit white man without significant past medical history who presented in stable condition complaining only of palpitations. He was found to have atrial flutter without rapid ventricular response on cardiac monitoring, most likely due to concomitant presence of high levels of nicotine and caffeine via chewing tobacco and energy drinks. He was treated conservatively with vagal maneuvers and intravenous fluids with complete resolution of symptoms and electrocardiographic abnormalities within 14 hours. This demonstrates an alternate conservative treatment strategy in appropriately risk stratified patients who present in an austere field setting with limited resources.


Assuntos
Flutter Atrial/induzido quimicamente , Cafeína/toxicidade , Nicotina/toxicidade , Adulto , Humanos , Masculino , População Rural
8.
Bratisl Lek Listy ; 121(3): 225-229, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32115981

RESUMO

AIM: Nicotine at high concentrations induces apoptosis in trophoblastic cells through induction of cell cytotoxicity and Reactive Oxygen Species (ROS). Methamphetamine in low dose has pharmaceutical properties. It seems that this components in low dose can protect the trophoblastic cells from nicotine-induced cell death. METHOD: Trophoblastic (JEG-3) cells grown in DMEM culture medium. MTT assay test detected the cell viability and Lactate Dehydrogenase test measured the cells cytotoxicity. Griess reaction was used for NO production analysis. Cell migration traced by wounding technique. Human Cytokine Array Focused 13-plex was also used for analysis of IL-1α, IL-1ß, IL-6, INFγ, and TNFα pre-inflammatory cytokines. RESULTS: Methamphetamine, in very low dose (pM), increased the cell viability and NO production, and decreased cell cytotoxicity, IL-1α, IL-1ß, IL-6, INFγ, and TNFα pre-inflammatory cytokines of JEG-3 cell which were exposed to high dose of nicotine, respectively. Cell migration was enhanced by low dose of methamphetamine in JEG-3 cells. CONCLUSION: Methamphetamine in very low dose suppressed the JEG-3 cell death induced by high dose of nicotine (Fig. 5, Ref. 48) Keywords: methamphetamine, nicotine, cell death, NO.


Assuntos
Dopaminérgicos , Inflamação , Metanfetamina , Trofoblastos , Linhagem Celular Tumoral , Sobrevivência Celular , Dopaminérgicos/farmacologia , Humanos , Inflamação/tratamento farmacológico , Metanfetamina/farmacologia , Nicotina/toxicidade , Trofoblastos/efeitos dos fármacos
9.
PLoS One ; 15(3): e0229637, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32134977

RESUMO

INTRODUCTION: Despite tobacco being an important preventable factor with respect to ill health and death, it is a legal substance that harms and kills many of those who use it. Text messaging smoking cessation interventions have been evaluated in a variety of contexts, and are generally considered to have a positive effect on smoking cessation success. In order for text messaging interventions to continue to be useful as prevalence of smoking decreases, it may be necessary to tailor the interventions to specific individuals. However, little is known with regard to who benefits the most and least from existing interventions. METHODS: In order to identify heterogenous treatment effects, we analyzed data from a randomized controlled trial of a text messaging smoking cessation intervention targeting university students in Sweden. We used a Bayesian hierarchical model where the outcome was modelled using logistic regression, and so-called horseshoe priors were used for coefficients. Predictive performance of the model, and heterogeneous treatment effects, were calculated using cross-validation over the trial data. RESULTS: Findings from the study of heterogenous treatment effects identified less effect of the intervention among university students with stronger dependence of nicotine and students who smoke a greater quantity of cigarettes per week. No heterogeneity was found with respect to sex, number of years smoking, or the use of snuff. DISCUSSION: Results emphasize that individuals with a more developed dependence of nicotine may have a harder time quitting smoking even with support. This questions the dissemination and development of text messaging interventions to university students in the future, as they may not be the optimal choice of intervention for those with a more developed dependence. On the other hand, text messaging interventions may be useful to disseminate among university students that are at risk of developing a strong dependence. TRIAL REGISTRATION: International Standard Randomized Controlled Trial Number (ISRCTN): 75766527; http://www.controlled-trials.com/ISRCTN75766527.


Assuntos
Abandono do Hábito de Fumar/métodos , Fumar/terapia , Estudantes/psicologia , Fumar Tabaco/terapia , Adulto , Teorema de Bayes , Terapia Comportamental/métodos , Feminino , Humanos , Masculino , Nicotina/administração & dosagem , Suécia , Envio de Mensagens de Texto , Tabaco sem Fumaça , Universidades , Adulto Jovem
10.
Evid Based Dent ; 21(1): 32-33, 2020 03.
Artigo em Inglês | MEDLINE | ID: mdl-32221495

RESUMO

Data sources The review included 42 pre-clinical in-vitro studies, published between 1995 and 2017. Study selection The study selected in-vitro studies which had assessed the effect of nicotine on human gingival and periodontal fibroblasts and epithelial cells. Typically, diluted pure nicotine was added to a cell culture medium in a variety of doses for a variety of time periods and the cells were then compared against a no-nicotine control. Outcomes assessed were: Cell viability, cell attachment or adhesion, cell proliferation or inflammatory mediator production. Studies were restricted to English language and full-text only.Data extraction and synthesis Two members of the review team screened abstracts and reviewed the full-texts independently. Disagreements regarding inclusion were resolved by discussion and consultation with the third author. Data were also extracted independently using a specifically designed data extraction form which included a quality assessment specifically designed for in-vitro studies. A narrative synthesis of the results was carried out.Results The included studies were heterogeneous in their designs, with a wide variety of cell types, concentrations of nicotine (1 nM to 100 mM), exposure times (30 minutes to four weeks), and assays used. All studies were assessed at being at high risk of bias due to lack of randomisation, allocation concealment, and blinding. No effect on cell viability was observed when the nicotine concentrations used were within the ranges observed in-vivo in smokers, nicotine replacement therapy users (NRT) and e-cigarette users. Cell viability was adversely affected only when concentrations of nicotine reached those observed in the saliva of smokeless tobacco users (>5 mM). However, periodontal ligament cells are not usually exposed to saliva in-vivo. Effects on cell attachment, cell proliferation and production of inflammatory mediators were reported at a wide range of concentrations, but the effects were contradictory. The authors make several recommendations for future research in this area, to improve the quality of the primary studies. Conclusions At the concentrations found in smokers and users of NRT including e-cigarettes, nicotine is unlikely to be toxic to human gingival and periodontal ligament cells in in-vitro. Higher concentrations of nicotine, of the levels observed in the saliva of smokeless tobacco users, have been shown to be cytotoxic in vitro.


Assuntos
Sistemas Eletrônicos de Liberação de Nicotina , Abandono do Hábito de Fumar , Células Epiteliais , Humanos , Nicotina , Ligamento Periodontal , Fumar , Dispositivos para o Abandono do Uso de Tabaco
11.
PLoS One ; 15(3): e0230656, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32214373

RESUMO

INTRODUCTION: Smoking is a strong risk factor for disease severity in Crohn's disease (CD) and cessation improves outcomes. The nicotine metabolite ratio (NMR) predicts cessation success with pharmacotherapy: varenicline doubles cessation over nicotine replacement therapy (NRT) for "normal", but not "slow" metabolizers. Varenicline side effects are heightened in slow metabolizers. Methods using NMR to optimize cessation pharmacotherapy have not been evaluated in CD. AIMS: We aim to determine the prevalence of smoking in a CD population and then assess these smokers' attitudes toward a personalized metabolism-informed care (MIC) approach to cessation. METHODS: In this observational study, we surveyed 1098 patients visiting an inflammatory bowel disease center about their smoking history. We then evaluated a subgroup of individuals with CD (n = 32) who participated in a randomized controlled trial of smoking cessation using MIC versus usual care. For MIC, medication selection was informed by the NMR (normal ≥0.31 vs. slow <0.31). The primary outcomes were intervention satisfaction and match rates between NMR and medication choice. RESULTS: The baseline prevalence of smoking in our CD population was 13%. Intervention participants reported high rates of satisfaction (85%) and chose a medication that matched their NMR result more often in the MIC group (100% vs. 64%, p = 0.01). Six of 16 (37.5%) patients prescribed varenicline discontinued due to side effects. CONCLUSION: MIC produced high rates of satisfaction and matching between NMR and medication in CD patients, supporting patient acceptance and feasibility of precision smoking cessation in this population. To reduce smoking in CD, therapies such as MIC are needed to maximize efficacy and minimize side effects.


Assuntos
Doença de Crohn/patologia , Nicotina/metabolismo , Abandono do Hábito de Fumar/métodos , Adulto , Bupropiona/efeitos adversos , Bupropiona/uso terapêutico , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Cooperação do Paciente , Projetos Piloto , Prevalência , Ensaios Clínicos Controlados Aleatórios como Assunto , Índice de Gravidade de Doença , Fumar/tratamento farmacológico , Fumar/epidemiologia , Dispositivos para o Abandono do Uso de Tabaco/efeitos adversos , Resultado do Tratamento , Vareniclina/efeitos adversos , Vareniclina/uso terapêutico
12.
Artigo em Inglês | MEDLINE | ID: mdl-32065955

RESUMO

Developing dissolution testing methods to measure the nicotine release profiles from smokeless tobacco products is valuable for product assessment and product-to-product comparisons. In this work, we developed a robust dissolution method to study the in vitro release of nicotine from smokeless tobacco products using the U.S. Pharmacopeia flow-through cell dissolution apparatus 4 (USP-4). We further developed and validated a sensitive Ultra Performance Liquid Chromatography coupled to Photodiode Array detector (UPLC-PDA) method for the accurate quantitation of the released nicotine into artificial saliva, which is our selected dissolution medium. We have successfully shown the applicability of the validated method by investigating the release profiles of nicotine from various commercial and CORESTA reference smokeless tobacco products [CRP 1.1 (Swedish-style snus pouch), CRP 2.1 (American-style loose moist snuff), CRP 4 (loose-leaf chewing tobacco) and CRP 4.1 (chopped loose-leaf chewing tobacco)]. Nicotine release profiles were analyzed by calculating the difference factor (f1) and similarity factor (f2) by adopting a methodology referenced in the Guidance for Industry from FDA's Center for Drug Evaluation and Research (CDER) and by fitting the release profile curves using a first order kinetic model. Nicotine release was found to be dependent on the form and cut of the smokeless tobacco products, with a slower release observed for snus and loose-leaf, compared to chopped and loose moist snuff smokeless tobacco. This dissolution methodology can be extended to measure and compare release of other constituents from smokeless tobacco products and has the potential for method standardization.


Assuntos
Cromatografia Líquida de Alta Pressão/métodos , Nicotina/análise , Tabaco sem Fumaça/análise , Técnicas de Química Analítica/instrumentação , Técnicas de Química Analítica/métodos , Desenho de Equipamento , Humanos , Limite de Detecção , Modelos Lineares , Modelos Biológicos , Nicotina/farmacocinética , Reprodutibilidade dos Testes , Saliva/química
13.
Rev Med Suisse ; 16(682): 357-360, 2020 Feb 19.
Artigo em Francês | MEDLINE | ID: mdl-32073770

RESUMO

In Switzerland, about 13  % of pregnant women smoke, giving birth to more than 11'000 infants per year exposed to tobacco in utero. Although this proportion is stable since the 2000's, the users of nicotine with new devices (electronic cigarettes, inhaled heated tobacco, sniffed or chewed tobacco) are increasing. The literature is unanimous about deleterious effects of prenatal exposure to tobacco smoke on the fetus, with multiple short- and long-term consequences. Available data suggest that in utero exposure to e-cigarette could also expose the fetus to a similar profile of adverse effects. In this article, we review briefly the known epidemiological and mechanistic data on the short- and long-term effects of prenatal cigarette smoke and nicotine consumption.


Assuntos
Sistemas Eletrônicos de Liberação de Nicotina , Exposição Materna/efeitos adversos , Nicotina/efeitos adversos , Efeitos Tardios da Exposição Pré-Natal/induzido quimicamente , Fumar/efeitos adversos , Produtos do Tabaco/efeitos adversos , Feminino , Humanos , Gravidez , Suíça
14.
Chemosphere ; 249: 126153, 2020 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-32058129

RESUMO

In this study, we determined DNA damage and chromosome breakage (indicators of genotoxicity) and cell viability (an indicator of cytotoxicity) in human lymphoblastoid TK6 and Chinese hamster ovary (CHO) cells treated with 33 e-liquids using in vitro single cell gel (comet), micronucleus (MN), and trypan blue assays, respectively. We also measured the contents of nicotine, five phthalate esters, and DL-menthol in the e-liquids to examine their effects on DNA damage, chromosome breakage, and cell viability. Our chemical analyses showed that: (1) six e-liquids had nicotine ≥2-fold higher than the manufacture's label claim (2-3.5 mg); (2) both dimethyl- and dibutyl-phthalate levels were >0.1 µg/g, i.e., their threshold limits as additives in cosmetics; and (3) the DL-menthol contents ranged from 0.0003 to 85757.2 µg/g, with those of two e-liquids being >1 mg/g, the threshold limit for trigging sensory irritation. Though all the e-liquids induced DNA damage in TK6 cells, 20 resulted in cell viabilities ≤75%, indicating cytotoxicity, yet the inverse relationship between cell viability and DNA damage (r = -0.628, p = 0.003) might reflect their role as pro-apoptotic and DNA damage inducers. Fifteen e-liquids induced MN% in TK6 cells ≥3-fold that of untreated cells. Some of the increase in %MN might be false due to high cytotoxicity, yet six brands showed acceptable cell viabilities (59-71%), indicating chromosome damage. DNA damage and %MN increased when the TK6 cells were exposed to metabolic activation. The CHO cells were less sensitive to the genotoxic effects of the e-liquids than the TK6 cells. DL-menthol was found to be associated with decreased cell viability and increased DNA damage, even at low levels. We cannot dismiss the presence of other ingredients in e-liquids with cytotoxic/genotoxic properties since out of the 63 different flavors, 47 induced DNA damage (≥3-folds), and 26 reduced cell viability (≤75%) in TK6 cells.


Assuntos
Vapor do Cigarro Eletrônico/química , Ácidos Ftálicos/química , Animais , Células CHO , Sobrevivência Celular/efeitos dos fármacos , Cricetinae , Cricetulus , Dano ao DNA , Dibutilftalato/farmacologia , Vapor do Cigarro Eletrônico/análise , Vapor do Cigarro Eletrônico/toxicidade , Ésteres/química , Humanos , Mentol/química , Mentol/toxicidade , Testes para Micronúcleos/métodos , Nicotina/química , Nicotina/toxicidade
15.
Mar Drugs ; 18(2)2020 Feb 11.
Artigo em Inglês | MEDLINE | ID: mdl-32053997

RESUMO

Many organisms possess "secondary" compounds to avoid consumption or to immobilize prey. While the most abundant or active compounds are initially investigated, more extensive analyses reveal other "minor" compounds with distinctive properties that may also be of biomedical and pharmaceutical significance. Here, we present an initial in vitro investigation of the actions of two isomeric tetrahydropyridyl ring-containing anabasine analogs: isoanatabine, an alkaloid isolated from a marine worm, and anatabine, a relatively abundant minor alkaloid in commercial tobacco plants. Both compounds have a double bond that is distal to the piperidine ring nitrogen of anabasine. Racemic isoanatabine and anatabine were synthesized and their S- and R-enantiomers were isolated by chiral high pressure liquid chromatography (HPLC). Both isoanatabines displayed higher efficacies at α4ß2 nicotinic acetylcholine receptors (nAChRs) relative to the anatabines; R-isoanatabine was most potent. Radioligand binding experiments revealed similar α4ß2 nAChR binding affinities for the isoanatabines, but R-anatabine affinity was twice that of S-anatabine. While the two anatabines and S-isoanatabine were highly efficacious agonists at α7 nAChRs, R-isoanatabine was only a weak partial agonist. The four compounds share an ability to stimulate both α4ß2 and α7 nAChRs, a property that may be useful in developing more efficacious drugs to treat neurodegenerative and other medical disorders.


Assuntos
Alcaloides/farmacologia , Anabasina/farmacologia , Agonistas Nicotínicos/farmacologia , Piridinas/farmacologia , Receptor Nicotínico de Acetilcolina alfa7/agonistas , Animais , Humanos , Isomerismo , Toxinas Marinhas , Nicotina , Receptores Nicotínicos , Tabaco
16.
Pneumologie ; 74(2): 77-87, 2020 Feb.
Artigo em Alemão | MEDLINE | ID: mdl-32016924

RESUMO

Beginning in April of 2019, the US saw > 2,000 cases of hospitalized, often young, patients with severe acute lung injury, of which over 40 died, and the only existing connection between patients was their use of electronic cigarettes (e-cigarettes). The acronym EVALI ("e-cigarette, or vaping, product use associated lung injury") has since been established for the condition. This review article is intended to provide an overview of recent, mainly US literature on EVALI, including the case definition, epidemiology, clinical presentation, typical disease progression, as well as potential triggers. Ancillary to this, the review further provides a general overview of the basic function of e-cigarettes, the ingredients of the liquids used in these (e-liquids), as well as a brief description of the associated potential inhalation risks.


Assuntos
Lesão Pulmonar Aguda/induzido quimicamente , Dronabinol/efeitos adversos , Sistemas Eletrônicos de Liberação de Nicotina , Vaping/efeitos adversos , Lesão Pulmonar Aguda/epidemiologia , Canabidiol/administração & dosagem , Canabidiol/efeitos adversos , Surtos de Doenças , Dronabinol/administração & dosagem , Humanos , Nicotina/administração & dosagem , Nicotina/efeitos adversos , Fatores de Risco
19.
Pediatrics ; 145(3)2020 03.
Artigo em Inglês | MEDLINE | ID: mdl-32047098

RESUMO

Recently, there has been a significant increase in the use of noncombustible nicotine-containing products, including electronic cigarettes (e-cigarettes). Of increasing popularity are e-cigarettes that can deliver high doses of nicotine over short periods of time. These devices have led to a rise in nicotine addiction in adolescent users who were nonsmokers. Use of noncombustible nicotine products by pregnant mothers is also increasing and can expose the developing fetus to nicotine, a known teratogen. In addition, young children are frequently exposed to secondhand and thirdhand nicotine aerosols generated by e-cigarettes, with little understanding of the effects these exposures can have on health. With the advent of these new nicotine-delivery systems, many concerns have arisen regarding the short- and long-term health effects of nicotine on childhood health during all stages of development. Although health studies on nicotine exposure alone are limited, educating policy makers and health care providers on the potential health effects of noncombustible nicotine is needed because public acceptance of these products has become so widespread. Most studies evaluating the effects of nicotine on health have been undertaken in the context of smoke exposure. Nevertheless, in vitro and in vivo preclinical studies strongly indicate that nicotine exposure alone can adversely affect the nervous, respiratory, immune, and cardiovascular systems, particularly when exposure occurs during critical developmental periods. In this review, we have included both preclinical and clinical studies to identify age-related health effects of nicotine exposure alone, examining the mechanisms underlying these effects.


Assuntos
Desenvolvimento Infantil/efeitos dos fármacos , Nicotina/efeitos adversos , Adolescente , Criança , Pré-Escolar , Humanos , Lactente , Recém-Nascido , Nicotina/metabolismo , Fumar/efeitos adversos , Poluição por Fumaça de Tabaco/efeitos adversos
20.
Life Sci ; 243: 117301, 2020 Feb 15.
Artigo em Inglês | MEDLINE | ID: mdl-31953160

RESUMO

AIM: Pancreatic stellate cells (PSCs) are the main functional cells leading to pancreatic fibrosis. Nicotine is widely considered as an independent risk factor of pancreatic fibrosis, but the mechanism is still unclear. Our study was aimed to explore the effects of nicotine on human pancreatic stellate cells (hPSCs) and involved pathways. MATERIALS AND METHODS: Primary human PSCs were cultured and treated with nicotine (0.1 µM and 1 µM). The proliferation, apoptosis, α-SMA expression, extracellular matrix metabolism and autophagy of hPSCs were detected by CCK-8 assay, flow cytometry, real-time PCR and Western blotting analysis. The α7nAChR-mediated JAK2/STAT3 signaling pathway was also examined, and an α7nAChR antagonist α-bungarotoxin (α-BTX) was used to perform inhibition experiments. KEY FINDINGS: The proliferation, α-SMA expression and autophagy of hPSCs were significantly promoted by 1 µM nicotine. Meanwhile, the apoptosis of hPSCs was significantly reduced. The extracellular matrix metabolism of hPSCs was also regulated by nicotine. Moreover, the α7nAChR-mediated JAK2/STAT3 signaling pathway was activated by nicotine, this pathway and effects of nicotine can be blocked by α-BTX. SIGNIFICANCE: Our finding suggests that nicotine can promote activation of human pancreatic stellate cells (hPSCs) through inducing autophagy via α7nAChR-mediated JAK2/STAT3 signaling pathway, providing a new insight into the mechanisms by which nicotine affects pancreatic fibrosis.


Assuntos
Autofagia/efeitos dos fármacos , Janus Quinase 2/metabolismo , Nicotina/farmacologia , Células Estreladas do Pâncreas/efeitos dos fármacos , Fator de Transcrição STAT3/metabolismo , Transdução de Sinais/efeitos dos fármacos , Receptor Nicotínico de Acetilcolina alfa7/metabolismo , Actinas/metabolismo , Células Cultivadas , Matriz Extracelular/efeitos dos fármacos , Matriz Extracelular/metabolismo , Humanos , Células Estreladas do Pâncreas/metabolismo
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