scholarly journals Jianpiyifei II Granules Suppress Apoptosis of Bronchial Epithelial Cells in Chronic Obstructive Pulmonary Disease via Inhibition of the Reactive Oxygen Species-Endoplasmic Reticulum Stress-Ca2+ Signaling Pathway

2020 ◽  
Vol 11 ◽  
Author(s):  
Long Fan ◽  
Leng Li ◽  
Xuhua Yu ◽  
Ziyao Liang ◽  
Tiantian Cai ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Chronic Obstructive Pulmonary Disease ◽  
Endoplasmic Reticulum ◽  
Epithelial Cells ◽  
Endoplasmic Reticulum Stress ◽  
Pulmonary Disease ◽  
Chronic Obstructive ◽  
Oxygen Species ◽  
Obstructive Pulmonary Disease ◽  
Bronchial Epithelial

Tobacco Smoking: Risk to Develop Addiction, Chronic Obstructive Pulmonary Disease, and Lung Cancer

2019 ◽  
Vol 14 (1) ◽  
pp. 39-52 ◽  
Author(s):  
Alessia Santoro ◽  
Carlo Tomino ◽  
Giulia Prinzi ◽  
Palma Lamonaca ◽  
Vittorio Cardaci ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Chronic Obstructive Pulmonary Disease ◽  
Epithelial Cells ◽  
Pulmonary Disease ◽  
Tobacco Smoking ◽  
Nicotinic Receptors ◽  
Bronchial Epithelial Cells ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Bronchial Epithelial

Background: The morbidity and mortality associated with tobacco smoking is well established. Nicotine is the addictive component of tobacco. Nicotine, through the non-neuronal α7nicotinic receptor, induces cell proliferation, neo-angiogenesis, epithelial to mesenchymal transition, and inhibits drug-induced apoptosis. Objective: To understand the genetic, molecular and cellular biology of addiction, chronic obstructive pulmonary disease and lung cancer. Methods: The search for papers to be included in the review was performed during the months of July- September 2018 in the following databases: PubMed (http://www.ncbi.nlm.nih.gov), Scopus (http://www.scopus.com), EMBASE (http://www.elsevier.com/online-tools/embase), and ISI Web of Knowledge (http://apps.webofknowledge.com/). The following searching terms: “nicotine”, “nicotinic receptor”, and “addiction” or “COPD” or “lung cancer” were used. </P><P> Patents were retrieved in clinicaltrials.gov (https://clinicaltrials.gov/). All papers written in English were evaluated. The reference list of retrieved articles was also reviewed to identify other eligible studies that were not indexed by the above-mentioned databases. </P><P> New experimental data on the ability of nicotine to promote transformation of human bronchial epithelial cells, exposed for one hour to Benzo[a]pyrene-7,8-diol-9-10-epoxide, are reported. Results: Nicotinic receptors variants and nicotinic receptors upregulation are involved in addiction, chronic obstructive pulmonary disease and/or lung cancer. Nicotine through α7nicotinic receptor upregulation induces complete bronchial epithelial cells transformation. Conclusion: Genetic studies highlight the involvement of nicotinic receptors variants in addiction, chronic obstructive pulmonary disease and/or lung cancer. A future important step will be to translate these genetic findings to clinical practice. Interventions able to help smoking cessation in nicotine dependence subjects, under patent, are reported.

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