Quzhou Aurantii Fructus Extract Attenuates Idiopathic Pulmonary Fibrosis by Regulating Nrf2/HO-1 Axis
Li Yu, Lixia Wang, Jinyao Zhang, Ruimin Sun, Siming Zhang, Ping Yin, Ying Chen, Guocan Chen, Yiping Ye, Haitong Wan, Yu He, Yunxiang Chen, Lijiang Zhang
Journal:Biology-Basel
IF:4.3
DOI:10.3390/biology15090716
PMID:42117855
Published:2026-04-30
research field:分子生物学药理学肺纤维化研究中医药学呼吸医学
Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressive fibrotic lung disease, and the available medications face challenges in reversing its course. Traditional Chinese medicine has been given wide publicity because of its minimal side effects and enormous potential. Quzhou Aurantii Fructus Extract (QAFE) was used in this study, and through mouse and cell-based experiments, QAFE suppressed inflammation, scarring, and cell damage due to IPF by stimulating the Nrf2/HO-1 pathway. The study findings are that QAFE can be used as an antifibrotic agent in the treatment of IPF. Recently, Quzhou Aurantii Fructus Extract (QAFE) was reported to exert anti-inflammatory effects on different types of respiratory diseases; however, it is yet to be determined whether it is effective in patients with idiopathic pulmonary fibrosis (IPF). The purpose of this study is to explore the capacity of QAFE to fight fibrotic disease, in particular how it works in relation to the regulation of the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) pathway. QAFE was made with Quzhou Fructus Aurantii (QAF), and the content of four flavonoids in the samples prepared was analyzed by high-performance liquid chromatography (HPLC). The therapeutic effect of QAFE was experimented by establishing IPF models in mice and in cells. Identification of the mechanism of QAFE in IPF through knockout or knockdown of the Nrf2 gene. The experiments suggest that QAFE has the potential to prevent IPF-induced inflammation, collagen deposition, oxidative stress, and apoptosis of cells. Silencing Nrf2 by knockdown or knockout is enough to prevent the capacity of QAFE to inhibit the process of inflammation, oxidative stress, and collagen deposition to cause more serious lung injury and HO-1 expression downregulation. QAFE is a potential new antifibrotic drug in IPF with an effect on the Nrf2/HO-1 pathway that reduces inflammation and oxidative stress.
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