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

## TL;DR

This study shows that tBHQ can reduce cell death caused by particulate matter in nasal cells, potentially helping treat sinus diseases.

## Contribution

The novel finding is that tBHQ inhibits PM-induced pyroptosis through the Nrf2 pathway in nasal epithelial cells.

## Key findings

- tBHQ inhibits PM-induced pyroptosis in nasal cells via the Nrf2 pathway.
- NLRP3 inflammasome activation is suppressed by tBHQ in a Nrf2-dependent manner.
- tBHQ shows therapeutic potential for PM-related sinonasal diseases.

## Abstract

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.