AI Article Synopsis
- Particulate matter 2.5 (PM) causes lung damage by ramping up the production of reactive oxygen species (ROS) and inflammation, activating pathways that lead to cell death.
- Treatment with 8-hydroxydeoxyguanosine (8-OHdG) reduces ROS and inflammation by lowering RAC1 activity and NOX expression in lung cells.
- Experiments show that 8-OHdG significantly lessens the harmful effects of PM on lung cells, indicating its potential as a therapeutic strategy for PM-induced lung injury.
Article Abstract
Particulate matter 2.5 (PM) induces lung injury by increasing the generation of reactive oxygen species (ROS) and inflammation. ROS aggravates NLRP3 inflammasome activation, which activates caspase-1, IL-1β, 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 PM-induced lung injury, we evaluated whether 8-OHdG decreased PM-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 μg/mL PM increased ROS generation, RAC1 activity, NOX1 expression, NLRP3 inflammasome (NLRP3, ASC, and caspase-1) activity, and IL-1β and IL-18 levels in cells; treatment with 10 μg/mL 8-OHdG significantly attenuated these effects. Furthermore, similar results, such as reduced expression of NOX1, NLRP3, ASC, and caspase-1, were observed in PM-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 PM.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10295443 | PMC |
| http://dx.doi.org/10.3390/antiox12061189 | DOI Listing |
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