Chronic Obstructive Pulmonary Disease (COPD) is a dangerous prevalent smoking-related disease characterized by abnormal inflammation and oxidative stress and expected to be the third cause of death in the world next decade. Corticosteroids have low effects in decreasing numbers of inflammatory mediators specifically in long-term use. Our study designed to investigate the possible protective effects of combined dexamethasone (Dex) (2mg/kg) and losartan (Los) (30mg/kg angiotensin receptor blocker, it possesses antioxidant and anti-inflammatory properties in lung injury in mice) against cigarette -smoke (CS) induced COPD in rats compared with dexamethasone and losartan. Male Sprague Dawley rats (N = 40) divided into five groups (n = 8): control group, CS group, Dex group, Los group, and Dex +Los group. COPD induced in rats by CS exposure twice daily for 10 weeks. After the specified treatment period, bronchoalveolar lavage fluid (BALF) and lung tissue were collected for measurement of SOD, NO, MDA, ICAM-, MMP-9, CRP, NF-κB and histopathology scoring. Our results indicated that Los+Dex significantly prevent CS-induced COPD emphysema, congested alveoli, and elevation of lung injury parameters in BALF. They also showed a significant decrease in MDA, ICAM-1, MMP-9, CRP, and NF-κB and a significant increase in SOD and NO. In conclusion, adding Los to Dex potentiating their activity in inhibition the progression of COPD based on its activity on oxidative stress, inflammation, and NF-κB protein expression.

慢性阻塞性肺疾病（COPD）是一种危险的、与吸烟相关的流行疾病，其特征是异常炎症和氧化应激，预计将成为未来十年世界第三大死亡原因。皮质类固醇在减少炎症介质数量方面效果较差，特别是长期使用时。我们的研究旨在调查地塞米松 (Dex) (2mg/kg) 和氯沙坦 (Los)（30mg/kg 血管紧张素受体阻滞剂，它在小鼠肺损伤中具有抗氧化和抗炎特性）联合使用对香烟的可能保护作用 -与地塞米松和氯沙坦相比，烟雾（CS）诱导大鼠慢性阻塞性肺病。雄性Sprague Dawley大鼠（N = 40）分为五组（n = 8）：对照组、CS组、Dex组、Los组和Dex +Los组。大鼠每天两次接触 CS 诱发慢性阻塞性肺病 (COPD)，持续 10 周。指定治疗时间后，收集支气管肺泡灌洗液（BALF）和肺组织，测定SOD、NO、MDA、ICAM-、MMP-9、CRP、NF-κB并进行组织病理学评分。我们的结果表明，Los+Dex 显着预防 CS 引起的 COPD 肺气肿、肺泡充血以及 BALF 中肺损伤参数的升高。他们还显示 MDA、ICAM-1、MMP-9、CRP 和 NF-κB 显着降低，SOD 和 NO 显着增加。总之，在 Dex 中添加 Los，基于其对氧化应激、炎症和 NF-κB 蛋白表达的活性，增强了其抑制 COPD 进展的活性。