Inflammatory response to chronic nicotine-containing electronic cigarette exposure in a rat model of myocardial infarction.

IF 1.9 4区 医学 Q2 PUBLIC, ENVIRONMENTAL & OCCUPATIONAL HEALTH
Tobacco Induced Diseases Pub Date : 2025-05-31 eCollection Date: 2025-01-01 DOI:10.18332/tid/204010
Jianru Shi, Wangde Dai, Juan Carreno, Jaspreet Sachdeva, Jesus Chavez, Michael T Kleinman, David A Herman, Rebecca J Arechavala, Irene Hasen, Amanda Ting, Robert A Kloner
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引用次数: 0

Abstract

Introduction: The long-term effects of chronic electronic cigarette (e-cigarette) exposure on lung and heart inflammation during the healing phase of myocardial infarction (MI) remain unexplored. Additionally, the impact of e-cigarette exposure on blood parameters in this context is unclear. This study aims to assess e-cigarette with nicotine (e-cig Nic+) effects on lung histology, inflammatory gene expression in cardiac tissue, and blood parameters during MI recovery.

Methods: Sprague Dawley rats of both sexes underwent proximal left coronary artery occlusion to induce a large anterior wall MI. After one week, rats were randomized to either air or e-cig Nic+ exposure for 12 weeks.

Results: In the lungs, e-cig Nic+ exposure led to a significant accumulation of inflammatory cells within the alveolar spaces and increased inflammatory cell numbers in the lung parenchyma compared to the air group. Numerically elevated levels of malondialdehyde (MDA), an oxidative stress biomarker, were observed in the e-cig Nic+ group. In the heart, a PCR array analysis of inflammatory cytokines and receptors revealed that 70 out of 84 inflammatory-related genes were downregulated in the e-cig Nic+ group, with 11 reaching statistical significance. Additionally, the blood of rats exposed to e-cig Nic+ exhibited significantly lower white blood cell, lymphocyte, and platelet counts compared to the air group.

Conclusions: Chronic exposure to e-cig Nic+ exacerbates lung inflammation, alters inflammatory gene expression in the heart, and suppresses immune cell counts in the blood during MI recovery. These findings suggest that e-cigarette with nicotine aerosol inhalation contributes to lung lesions and dampens immune and inflammatory responses in an already compromised MI setting.

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慢性含尼古丁电子烟暴露在大鼠心肌梗死模型中的炎症反应。
在心肌梗死(MI)愈合阶段,慢性电子烟(电子烟)暴露对肺和心脏炎症的长期影响尚不清楚。此外,在这种情况下,电子烟暴露对血液参数的影响尚不清楚。本研究旨在评估含尼古丁电子烟(电子烟Nic+)对心肌梗死恢复期间肺组织学、心脏组织炎症基因表达和血液参数的影响。方法:采用左冠状动脉近端闭塞术,诱导大鼠前壁心肌梗死。1周后,将大鼠随机分为空气暴露组和电子烟暴露组,连续12周。结果:在肺中,与空气组相比,电子烟暴露导致肺泡间隙内炎症细胞明显积聚,肺实质炎症细胞数量增加。在电子烟Nic+组中,观察到氧化应激生物标志物丙二醛(MDA)的数值升高。在心脏中,对炎症细胞因子和受体的PCR阵列分析显示,在电子烟Nic+组中,84个炎症相关基因中有70个下调,其中11个达到统计学意义。此外,与空气组相比,暴露于电子烟中的大鼠血液中白细胞、淋巴细胞和血小板计数明显降低。结论:慢性暴露于电子烟Nic+会加重肺部炎症,改变心脏炎症基因表达,并抑制心肌梗死恢复期血液中免疫细胞计数。这些发现表明,吸入尼古丁气溶胶的电子烟会导致肺部病变,并在已经受损的心肌梗死环境中抑制免疫和炎症反应。
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来源期刊
Tobacco Induced Diseases
Tobacco Induced Diseases SUBSTANCE ABUSE-PUBLIC, ENVIRONMENTAL & OCCUPATIONAL HEALTH
CiteScore
5.30
自引率
5.40%
发文量
95
审稿时长
12 weeks
期刊介绍: Tobacco Induced Diseases encompasses all aspects of research related to the prevention and control of tobacco use at a global level. Preventing diseases attributable to tobacco is only one aspect of the journal, whose overall scope is to provide a forum for the publication of research articles that can contribute to reducing the burden of tobacco induced diseases globally. To address this epidemic we believe that there must be an avenue for the publication of research/policy activities on tobacco control initiatives that may be very important at a regional and national level. This approach provides a very important "hands on" service to the tobacco control community at a global scale - as common problems have common solutions. Hence, we see ourselves as "connectors" within this global community. The journal hence encourages the submission of articles from all medical, biological and psychosocial disciplines, ranging from medical and dental clinicians, through health professionals to basic biomedical and clinical scientists.
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