Molecular nutrition and food research
5.2
2093-8551
SCIE
[논문]Oral administration of Sargassum horneri suppresses particulate matter-induced oxidative DNA damage in alveolar macrophages of allergic airway inflammation: Relevance to PM-mediated M1/M2 AM polarization
Hyo Jin Kim
김효진
Jiwon Yang, Kalahe Hewage Iresha Nadeeka Madushani Herath, You-Jin Jeon, Young-Ok Son, Doyoung Kwon, Hyun Jung Kim, Youngheun Jee
Scope Particulate matter (PM) can cause cellular oxidative damage and promote respiratory diseases. It has recently shown that Sargassum horneri ethanol extract (SHE) containing sterols and gallic acid reduces PM‐induced oxidative stress in mice lung cells through ROS scavenging and metal chelating. In this study, the role of alveolar macrophages (AMs) is identified that are particularly susceptible to DNA damage due to PM‐triggered oxidative stress in lungs of OVA‐sensitized mice exposed to PM. Methods and results The study scrutinizes if PM exposure causes oxidative DNA damage to AMs differentially depending on their type of polarization. Further, SHE's potential is investigated in reducing oxidative DNA damage in polarized AMs and restoring AM polarization in PM‐induced allergic airway inflammation. The study discovers that PM triggers prolonged oxidative stress to AMs, leading to lipid peroxidation in them and alveolar epithelial cells. Particularly, AMs are polarized to M2 phenotype (F4/80 ⁺ CD206 ⁺ ) with enhanced oxidative DNA damage when subject to PM‐induced oxidative stress. However, SHE repairs oxidative DNA damage in M1‐ and M2‐polarized AMs and reduces AMs polarization imbalance due to PM exposure. Conclusion These results suggest the possibility of SHE as beneficial foods against PM‐induced allergic airway inflammation via suppression of AM dysfunction.
2023.11.20.
기타
논문 그래픽 동영상
2023-12-15
저작자표시-비영리
이 데이터의 저작권은 <연구자 기관/그룹/사용자>에게 있습니다.
관리자 ( 2023-12-15 ) [논문]Oral administration of Sargassum horneri suppresses particulate matter-induced oxidative DNA damage in alveolar macrophages of allergic airway inflammation: Relevance to PM-mediated M1/M2 AM polarization