Alterations in Adiponectin Expression in Models of Cigarette Smoke Extract-Induced Mouse Pulmonary Emphysema and Alveolar Epithelial Cell Injury.

IF 2.2 4区医学 Q3 RESPIRATORY SYSTEM

COPD: Journal of Chronic Obstructive Pulmonary Disease Pub Date : 2025-03-06 Epub Date: 2025-03-13 DOI:10.1080/15412555.2025.2477235

Siriporn Vongsaiyat Siriphorn, Supitsara Thorsuwan, Julalux Thongam, Sukpattaraporn Ruangklai, Poungpetch Hussarin, Thanaporn Rungruang, Sorachai Srisuma

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引用次数: 0

Abstract

Purpose: Cigarette smoke activates lung inflammation and destruction and the development of COPD. Among various factors influenced by lung inflammation, adiponectin produced by lung epithelial cells is thought to play a significant role in regulating inflammation and maintaining tissue integrity. This study aims to examine adiponectin expression in a mouse model of cigarette smoke extract (CSE)-induced emphysema and explore the effects of adiponectin on cell survival and cytokine gene expression in CSE-induced lung epithelial cell damage.

Methods: CSE was prepared by passing cigarette smoke through a glass tube containing solvent. PBS or CSE was intraperitoneally administered to C57BL/6 mice. Inflammatory cells, cytokines, adiponectin expression in lung, bronchoalveolar lavage fluid (BALF) and adipose tissue were assessed. CSE and adiponectin were administered to A549 cells to determine cell viability and cytokine gene expression.

Results: Intraperitoneal CSE injection significantly increased the mean alveolar linear intercept by 23.11%. CSE significantly increased total cells, macrophages, neutrophils, eosinophils, TNFα, IL-1β levels in BALF. CSE enhanced lung adiponectin protein expression. Treatment of A549 cells with CSE reduced cell survival and adiponectin gene expression. Furthermore, adiponectin treatment enhanced MCP-1 and IL-8 gene expression in A549 cells post-CSE exposure.

Conclusion: Intraperitoneal CSE treatment induced lung inflammation, airspace enlargement, and increased adiponectin expression in mice. CSE-exposed A549 cells showed reduced cell viability, upregulated proinflammatory genes, downregulated adiponectin genes. Adiponectin treatment further intensified these genes expressions, aligning with in vivo findings. Elevated adiponectin expression in alveolar epithelial cells suggests its potential role in the development of COPD by enhancing lung inflammation.

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香烟烟雾提取物诱导小鼠肺气肿和肺泡上皮细胞损伤模型中脂联素表达的变化。

目的：香烟烟雾激活肺部炎症和破坏，促进慢性阻塞性肺病的发展。在肺部炎症影响的多种因素中，肺上皮细胞产生的脂联素被认为在调节炎症和维持组织完整性方面发挥重要作用。本研究旨在检测脂联素在香烟烟雾提取物（CSE）诱导的小鼠肺气肿模型中的表达，探讨脂联素对烟雾提取物诱导的肺上皮细胞损伤中细胞存活和细胞因子基因表达的影响。方法：用含溶剂的玻璃管传烟制备CSE。C57BL/6小鼠腹腔注射PBS或CSE。观察肺、支气管肺泡灌洗液（BALF）和脂肪组织中炎症细胞、细胞因子、脂联素的表达。给A549细胞注射CSE和脂联素，检测细胞活力和细胞因子基因表达。结果：腹腔注射CSE显著提高平均肺泡线性截距23.11%。CSE显著提高了BALF中总细胞、巨噬细胞、中性粒细胞、嗜酸性粒细胞、TNFα、IL-1β水平。CSE增强肺脂联素蛋白表达。用CSE处理A549细胞可降低细胞存活率和脂联素基因表达。此外，脂联素处理增强了cse暴露后A549细胞中MCP-1和IL-8基因的表达。结论：腹腔注射CSE可引起小鼠肺部炎症、肺泡增大、脂联素表达升高。暴露于cse的A549细胞显示细胞活力降低，促炎基因上调，脂联素基因下调。脂联素治疗进一步增强了这些基因的表达，与体内研究结果一致。肺泡上皮细胞中脂联素表达升高提示其通过增强肺部炎症在COPD发展中的潜在作用。

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来源期刊

COPD: Journal of Chronic Obstructive Pulmonary Disease RESPIRATORY SYSTEM-

CiteScore

4.40

自引率

0.00%

发文量

审稿时长

6-12 weeks

期刊介绍： From pathophysiology and cell biology to pharmacology and psychosocial impact, COPD: Journal Of Chronic Obstructive Pulmonary Disease publishes a wide range of original research, reviews, case studies, and conference proceedings to promote advances in the pathophysiology, diagnosis, management, and control of lung and airway disease and inflammation - providing a unique forum for the discussion, design, and evaluation of more efficient and effective strategies in patient care.