Oxidant Stress & Apoptosis in Chronic Cigarette Exposure

氧化应激

• 批准号: 7245117
• 负责人: ALISON JONES MONTPETIT
• 金额: $ 3万
• 依托单位: UNIVERSITY OF SOUTH FLORIDA
• 依托单位国家: 美国
• 财政年份: 2005
• 资助国家: 美国
• 起止时间: 2005-08-19 至 2009-08-18
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7245117
• 关键词: antioxidants; apoptosis; atrial natriuretic peptide; biotechnology; bronchus; cell line; cellular pathology; clinical research; cytoprotection; free radical oxygen; gene expression; glutathione; microarray technology; necrosis; organ culture; oxidative stress; pathologic process; predoctoral investigator; protein engineering; recombinant proteins; respiratory epithelium; respiratory pharmacology; smoking; tobacco abuse; transfection /expression vector

DESCRIPTION (provided by applicant): Lung disease is the third leading cause of death in the US. Nurses provide symptom management of lung disease by promoting smoking cessation for relief of dyspnea. Unfortunately, many continue to smoke despite the risk of pulmonary disease or disease exacerbation. In addition, the mechanisms of cigarette smoke induced pulmonary disease are not well known. This research will apply a conceptual model to study the effects of cigarette induced oxidant stress on gene expression, apoptosis, and oxidant stress measures in a normal human bronchial epithelial (NHBE) 3D in vitro model. In addition, this study seeks to elucidate the potential bronchoprotective effects of a novel natriuretic peptide (NHP 73-102). This proposal is a series of factorial design experiments. 3D NHBE cell cultures will be transfected with an NHP73-102 gene expression vector and exposed to cigarette smoke condensate (CSC). Microarray gene expression data, apoptosis/necrosis, and oxidant stress measures will be assessed and evaluated by cluster analysis and ANOVA (ANalysis Of VAriance) between groups respectively. The information gained in this study will provide unique data related to the effects of cigarette-induced oxidant stress and insight into the physiological mechanisms of NHP73-102 in the lung.

描述（由申请人提供）：肺部疾病是美国第三大死亡原因。护士通过促进戒烟缓解呼吸困难来提供肺部疾病的症状管理。不幸的是，许多人继续吸烟，尽管肺部疾病或疾病恶化的风险。此外，吸烟引起的肺部疾病的机制还不清楚。本研究将应用概念模型研究香烟诱导的氧化应激对正常人支气管上皮（NHBE）3D体外模型中基因表达、细胞凋亡和氧化应激措施的影响。此外，本研究旨在阐明一种新型利钠肽（NHP 73-102）的潜在支气管保护作用。本方案是一系列析因设计实验。3D NHBE细胞培养物将用NHP 73 -102基因表达载体转染并暴露于香烟烟雾冷凝物（CSC）。将分别通过组间聚类分析和ANOVA（方差分析）评估和评价微阵列基因表达数据、细胞凋亡/坏死和氧化应激指标。本研究中获得的信息将提供与蒙脱石诱导的氧化应激的影响相关的独特数据，并深入了解NHP 73 -102在肺中的生理机制。