Artemisia gmelinii Extract Attenuates Particulate Matter-Induced Neutrophilic Inflammation in a Mouse Model of Lung Injury

Author:

Song Hyeon-Ji12,Shin Dong-Uk13,Eom Ji-Eun1ORCID,Lim Kyung Min13,Lim Eun Yeong1,Kim Young In1,Kim Ha-Jung12,Song Ju Hye13,Shim MyeongKuk4,Choe HyeonJeong4,Kim Gun-Dong1,Lee So-Young13,Shin Hee Soon13ORCID

Affiliation:

1. Division of Food Functionality Research, Korea Food Research Institute (KFRI), Wanju 55365, Republic of Korea

2. Department of Food Science and Technology, Jeonbuk National University, Jeonju 54896, Republic of Korea

3. Department of Food Biotechnology, Korea University of Science and Technology (UST), Daejeon 34113, Republic of Korea

4. BL Healthcare Corp., Yongin 16827, Republic of Korea

Abstract

Particulate matter (PM) induces and augments oxidative stress and inflammation, leading to respiratory diseases. Although Artemisia gmelinii Weber ex Stechm has antioxidant and anti-inflammatory effects, there are no reports on whether Artemisia gmelinii extract (AGE) regulates lung inflammation in a PM-induced model. Thus, we investigated the protective effects of AGE using a PM-induced mouse lung inflammation model. AGE significantly decreased the expression of inflammatory chemokines, neutrophil extracellular trap formation, and the total number of inflammatory cells in the bronchoalveolar lavage fluid (BALF). Furthermore, AGE attenuated lung inflammation through the suppression of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)/mitogen-activated protein kinase (MAPK) signaling pathway, while promoting the nuclear factor erythroid-2-related factor 2 (NRF2)/heme oxygenase-1 (HO-1) signaling pathway in lung tissues. Concordant with these observations, AGE suppressed inflammatory cytokines, chemokines, reactive oxygen species, NETosis, myeloperoxidase, and neutrophil elastase by decreasing the mRNA expression of High mobility group box 1, Runt-related transcription factor 1, and Kruppel-like factor 6 in differentiated HL-60 cells. In summary, our data demonstrated that AGE suppresses PM-induced neutrophil infiltration, lung damage, and pulmonary inflammation by suppressing NF-κB/MAPK signaling pathways and enhancing the NRF2/HO-1 signaling pathway. These findings suggest that AGE administration is an effective approach for preventing and treating PM-induced respiratory inflammation.

Funder

Ministry of Science and ICT

Publisher

MDPI AG

Subject

Cell Biology,Clinical Biochemistry,Molecular Biology,Biochemistry,Physiology

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