Department of Respiration, First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, Zhejiang, People's Republic of China.
Inflammation. 2018 Oct;41(5):1671-1680. doi: 10.1007/s10753-018-0811-x.
The aim of this study was to investigate the effects of Astragaloside IV (AS) on cigarette smoke (CS)-induced chronic obstructive pulmonary disease (COPD). Our results showed that AS alleviated CS-induced pathological injury in lung tissue. AS also increased superoxide dismutase (SOD) and reduced the level of malondialdehyde (MDA) in serum and lung. AS also reduced cytokines including tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) in serum and lung. More, AS significantly reduced the protein expression of JAK3/STAT3/NF-κB pathway in CS-induced mice. In vitro, cigarette smoke extract (CSE) stimulation exposed to normal human bronchial epithelial (HBE) cells. Results further confirmed that AS significantly inhibited the protein levels of JAK3/STAT3/NF-κB pathway in CSE-induced HBE. Our result showed that AS might effectively ameliorate COPD via JAK3/STAT3/NF-κB pathway.
本研究旨在探讨黄芪甲苷（AS）对香烟烟雾（CS）诱导的慢性阻塞性肺疾病（COPD）的影响。我们的结果表明，AS 减轻了 CS 诱导的肺组织病理损伤。AS 还增加了血清和肺中超氧化物歧化酶（SOD）的水平，降低了丙二醛（MDA）的水平。AS 还降低了血清和肺中的细胞因子，包括肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）和白细胞介素-1β（IL-1β）。此外，AS 还显著降低了 CS 诱导的小鼠 JAK3/STAT3/NF-κB 通路的蛋白表达。在体外，香烟烟雾提取物（CSE）刺激正常的人支气管上皮（HBE）细胞。结果进一步证实，AS 显著抑制了 CSE 诱导的 HBE 中 JAK3/STAT3/NF-κB 通路的蛋白水平。我们的结果表明，AS 可能通过 JAK3/STAT3/NF-κB 通路有效改善 COPD。
