Exogenous 8-Hydroxydeoxyguanosine Attenuates PM2.5-Induced Inflammation in Human Bronchial Epithelial Cells by Decreasing NLRP3 Inflammasome Activationopen access
- Authors
- Bang, Jihye; Son, Kuk Hui; Heo, Hye-Ryeon; Park, Eunsook; Kwak, Hyun-Jeong; Uhm, Kyung-Ok; Chung, Myung-Hee; Kim, Young-Youl; Lim, Hyun Joung
- Issue Date
- Jun-2023
- Publisher
- MDPI
- Keywords
- particulate matter 2; 5; lung injury; reactive oxygen species; 8-hydroxydeoxyguanosine; NLRP3 inflammasome
- Citation
- ANTIOXIDANTS, v.12, no.6
- Journal Title
- ANTIOXIDANTS
- Volume
- 12
- Number
- 6
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/88546
- DOI
- 10.3390/antiox12061189
- ISSN
- 2076-3921
- Abstract
- Particulate matter 2.5 (PM2.5) induces lung injury by increasing the generation of reactive oxygen species (ROS) and inflammation. ROS aggravates NLRP3 inflammasome activation, which activates caspase-1, IL-1 & beta;, and IL-18 and induces pyroptosis; these factors propagate inflammation. In contrast, treatment with exogenous 8-hydroxydeoxyguanosine (8-OHdG) decreases RAC1 activity and eventually decreases dinucleotide phosphate oxidase (NOX) and ROS generation. To establish modalities that would mitigate PM2.5-induced lung injury, we evaluated whether 8-OHdG decreased PM2.5-induced ROS generation and NLRP3 inflammasome activation in BEAS-2B cells. CCK-8 and lactate dehydrogenase assays were used to determine the treatment concentration. Fluorescence intensity, Western blotting, enzyme-linked immunosorbent assay, and immunoblotting assays were also performed. Treatment with 80 & mu;g/mL PM2.5 increased ROS generation, RAC1 activity, NOX1 expression, NLRP3 inflammasome (NLRP3, ASC, and caspase-1) activity, and IL-1 & beta; and IL-18 levels in cells; treatment with 10 & mu;g/mL 8-OHdG significantly attenuated these effects. Furthermore, similar results, such as reduced expression of NOX1, NLRP3, ASC, and caspase-1, were observed in PM2.5-treated BEAS-2B cells when treated with an RAC1 inhibitor. These results show that 8-OHdG mitigates ROS generation and NLRP3 inflammation by inhibiting RAC1 activity and NOX1 expression in respiratory cells exposed to PM2.5.
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