Department of Respiratory and Critical Care, Hebei Chest Hospital, Hebei 050048, China.
Department of Gynecology, Shijiazhuang Second Hospital, Shijiazhuang 050048, China.
Exp Biol Med (Maywood). 2020 Feb;245(3):190-200. doi: 10.1177/1535370220904342. Epub 2020 Feb 2.
Smoking has become a major cause of chronic obstructive pulmonary disease through weakening of the respiratory mucus-ciliary transport system, impairing cough reflex sensitivity, and inducing inflammation. Recent researches have indicated that hydrogen sulfide is essential in the development of various lung diseases. However, the effect and mechanism of hydrogen sulfide on cigarette smoke-induced chronic obstructive pulmonary disease have not been reported. In this study, rats were treated with cigarette smoke to create a chronic obstructive pulmonary disease model followed by treatment with a low concentration of hydrogen sulfide. Pulmonary function, histopathological appearance, lung edema, permeability, airway remodeling indicators, oxidative products/antioxidases levels, inflammatory factors in lung, cell classification in bronchoalveolar lavage fluid were measured to examine the effect of hydrogen sulfide on chronic obstructive pulmonary disease model. The results showed that hydrogen sulfide effectively improved pulmonary function and reduced histopathological changes, lung edema, and permeability. Airway remodeling, oxidative stress, and inflammation were also reduced by hydrogen sulfide treatment. To understand the mechanisms, we measured the expression of TGF-β1, TGF-βIand TGF-βII receptors and Smad7 and phosphorylation of Smad2/Smad3. The results indicated that the TGF-β1 and Smad were activated in cigarette smoke-induced chronic obstructive pulmonary disease model, but inhibited by hydrogen sulfide. In conclusion, this study showed that hydrogen sulfide treatment alleviated cigarette smoke-induced chronic obstructive pulmonary disease through inhibition of the TGF-β1/Smad pathway.
COPD has become a severe public health issue in the world and smoking has become a major cause of COPD. As a result, it is a demandingly needed to explore new potential therapy for cigarette smoke-associated COPD. The present study suggested that HS treatment improved pulmonary function and reduced histopathological changes, lung edema, permeability, inflammation, airway remodeling and oxidative injury in a COPD model induced by cigarette smoke. Although additional studies are required to elucidate the pharmacodynamics, pharmacokinetics, and pharmacology of HS in the cigarette smoke-associated COPD, our findings provide an experimental basis for the potential clinical application of HS in COPD treatment.
吸烟已成为慢性阻塞性肺疾病（COPD）的主要病因，其通过削弱呼吸黏液-纤毛转运系统、损害咳嗽反射敏感性和诱导炎症来实现。最近的研究表明，硫化氢在各种肺部疾病的发展中是必不可少的。然而，硫化氢对香烟烟雾诱导的慢性阻塞性肺疾病的影响及其机制尚未报道。在这项研究中，用香烟烟雾处理大鼠以建立慢性阻塞性肺疾病模型，然后用低浓度的硫化氢进行处理。测量肺功能、组织病理学表现、肺水肿、通透性、气道重塑指标、氧化产物/抗氧化酶水平、肺中的炎症因子、支气管肺泡灌洗液中的细胞分类，以检查硫化氢对慢性阻塞性肺疾病模型的影响。结果表明，硫化氢可有效改善肺功能，减轻组织病理学改变、肺水肿和通透性。气道重塑、氧化应激和炎症也因硫化氢处理而减轻。为了了解其机制，我们测量了 TGF-β1、TGF-βI 和 TGF-βII 受体以及 Smad7 和 Smad2/Smad3 的磷酸化表达。结果表明，香烟烟雾诱导的慢性阻塞性肺疾病模型中 TGF-β1 和 Smad 被激活，但被硫化氢抑制。总之，这项研究表明，硫化氢通过抑制 TGF-β1/Smad 通路来缓解香烟烟雾诱导的慢性阻塞性肺疾病。
