TBHQ Alleviates Particulate Matter-Induced Pyroptosis in Human Nasal Epithelial Cells.
Ji-Sun KimHyunsu ChoiJeong-Min OhSung Won KimSoo Whan KimByung Guk KimJin Hee ChoJoohyung LeeDong Chang LeePublished in: Toxics (2024)
Pyroptosis represents a type of cell death mechanism notable for its cell membrane disruption and the subsequent release of proinflammatory cytokines. The Nod-like receptor family pyrin domain containing inflammasome 3 (NLRP3) plays a critical role in the pyroptosis mechanism associated with various diseases resulting from particulate matter (PM) exposure. Tert-butylhydroquinone (tBHQ) is a synthetic antioxidant commonly used in a variety of foods and products. The aim of this study is to examine the potential of tBHQ as a therapeutic agent for managing sinonasal diseases induced by PM exposure. The occurrence of NLRP3 inflammasome-dependent pyroptosis in RPMI 2650 cells treated with PM < 4 µm in size was confirmed using Western blot analysis and enzyme-linked immunosorbent assay results for the pyroptosis metabolites IL-1β and IL-18. In addition, the inhibitory effect of tBHQ on PM-induced pyroptosis was confirmed using Western blot and immunofluorescence techniques. The inhibition of tBHQ-mediated pyroptosis was abolished upon nuclear factor erythroid 2-related factor 2 (Nrf2) knockdown, indicating its involvement in the antioxidant mechanism. tBHQ showed potential as a therapeutic agent for sinonasal diseases induced by PM because NLRP3 inflammasome activation was effectively suppressed via the Nrf2 pathway.
Keyphrases
- nlrp inflammasome
- particulate matter
- air pollution
- oxidative stress
- nuclear factor
- cell death
- diabetic rats
- high glucose
- endothelial cells
- induced apoptosis
- toll like receptor
- cell cycle arrest
- south africa
- immune response
- risk assessment
- drug induced
- high throughput
- chronic rhinosinusitis
- inflammatory response
- climate change
- mouse model
- induced pluripotent stem cells
- newly diagnosed
- pluripotent stem cells