TBHQ Alleviates Particulate Matter-Induced Pyroptosis in Human Nasal Epithelial Cells

Area of Science:

• Cellular Biology
• Toxicology
• Immunology

Background:

• Pyroptosis is a pro-inflammatory cell death mechanism crucial in diseases linked to particulate matter (PM) exposure.
• The NLRP3 inflammasome pathway is a key mediator of PM-induced pyroptosis.
• Sinonasal diseases can result from PM exposure, necessitating therapeutic interventions.

Purpose of the Study:

• To investigate the therapeutic potential of tert-butylhydroquinone (tBHQ) in mitigating PM-induced sinonasal inflammation.
• To elucidate the role of the NLRP3 inflammasome and Nrf2 pathway in tBHQ's protective effects.

Main Methods:

• Western blot and ELISA were used to confirm PM-induced pyroptosis and measure IL-1β and IL-18 levels.
• Immunofluorescence and Western blot assessed tBHQ's inhibitory effects on pyroptosis.
• Nrf2 knockdown experiments were performed to determine pathway involvement.

Main Results:

• PM exposure triggered NLRP3 inflammasome-dependent pyroptosis in RPMI 2650 cells.
• tBHQ significantly inhibited PM-induced pyroptosis.
• The inhibitory effect of tBHQ was dependent on the Nrf2 pathway, as Nrf2 knockdown abolished the effect.

Conclusions:

• tBHQ demonstrates potential as a therapeutic agent for PM-induced sinonasal diseases.
• tBHQ suppresses NLRP3 inflammasome activation through the Nrf2-dependent antioxidant pathway.
• Targeting the Nrf2 pathway may be a viable strategy for managing PM-related sinonasal conditions.