Suppr超能文献

金丝桃苷减轻博来霉素诱导的小鼠肺纤维化进展

Hyperoside Attenuates Bleomycin-Induced Pulmonary Fibrosis Development in Mice.

作者信息

Huang Jizhen, Tong Xiang, Zhang Li, Zhang Yuan, Wang Lei, Wang Dongguang, Zhang Shijie, Fan Hong

机构信息

Department of Respiratory and Critical Care Medicine, West China Hospital/West China School of Medicine, Sichuan University, Chengdu, China.

Department of Ophthalmology, Renmin Hospital of Wuhan University, Wuhan, China.

出版信息

Front Pharmacol. 2020 Oct 22;11:550955. doi: 10.3389/fphar.2020.550955. eCollection 2020.

Abstract

Idiopathic pulmonary fibrosis (IPF) is a progressive, lethal, and chronic lung disease. There are no effective drug therapies for IPF. Hyperoside, a flavonoid glycoside, has been proven to have anti-inflammatory, anti-fibrosis, antioxidant, and anti-cancer effects. The aim of this study was to explore the role of hyperoside in bleomycin-induced pulmonary fibrosis development in mice. We established the pulmonary fibrosis model by a single intratracheal aerosol injection of bleomycin. Seven days after the bleomycin treatment, the mice were intraperitoneally administered with hyperoside for 14 days. We found that hyperoside treatment ameliorated fibrotic pathological changes and collagen deposition in the lungs of mice with bleomycin-induced pulmonary fibrosis. Hyperoside treatment also reduced the levels of MDA, TNF-α, and IL-6 and increased the activity of SOD. In addition, hyperoside might inhibit the epithelial-mesenchymal transition (EMT) the AKT/GSK3β pathway. Based on these findings, hyperoside attenuated pulmonary fibrosis development by inhibiting oxidative stress, inflammation, and EMT in the lung tissues of mice with pulmonary fibrosis. Therefore, hyperoside might be a promising candidate drug for the treatment of pulmonary fibrosis.

摘要

特发性肺纤维化(IPF)是一种进行性、致命的慢性肺部疾病。目前尚无针对IPF的有效药物治疗方法。金丝桃苷是一种黄酮苷,已被证明具有抗炎、抗纤维化、抗氧化和抗癌作用。本研究的目的是探讨金丝桃苷在博来霉素诱导的小鼠肺纤维化发展中的作用。我们通过气管内单次雾化注射博来霉素建立了肺纤维化模型。博来霉素治疗7天后,给小鼠腹腔注射金丝桃苷,持续14天。我们发现,金丝桃苷治疗改善了博来霉素诱导的肺纤维化小鼠肺部的纤维化病理变化和胶原沉积。金丝桃苷治疗还降低了丙二醛(MDA)、肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)的水平,并增加了超氧化物歧化酶(SOD)的活性。此外,金丝桃苷可能通过AKT/糖原合成酶激酶3β(GSK3β)途径抑制上皮-间质转化(EMT)。基于这些发现,金丝桃苷通过抑制肺纤维化小鼠肺组织中的氧化应激、炎症和EMT,减轻了肺纤维化的发展。因此,金丝桃苷可能是一种有前途的治疗肺纤维化的候选药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1b4/7642689/2dd8a6bf428d/fphar-11-550955-g001.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验