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Polystyrene nanoplastics induce oral epithelial barrier dysfunction through suppression of CaMKKβ-AMPKα1 signaling, which is restored by pinoresinol in TR146 cells.
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In lab-grown human oral cells, exposure to polystyrene nanoplastics weakened the cell barrier by disrupting junction proteins and suppressing a cell signaling pathway called CaMKKβ-AMPKα1. A plant compound called pinoresinol restored barrier function and reactivated this signaling pathway in the same cells.
Microplastics and nanoplastics (MNPs) have emerged as widespread environmental contaminants that may interact with epithelial surfaces and compromise barrier integrity. The oral epithelium represents a continuous first-contact exposure interface for these particles; however, the mechanisms underlying nanoplastic-induced barrier dysfunction and associated epithelial stress responses remain poorly understood. This study investigated the effects of polystyrene nanoplastics (PSNPs) on epithelial barrier function in human TR146 oral epithelial cells and evaluated the protective role of the polyphenol pinoresinol. PSNPs exposure resulted in a sub-cytotoxic reduction in cell viability but significantly impaired epithelial barrier function, as indicated by increased fluorescein isothiocyanate-dextran (FD4) permeability and decreased transepithelial electrical resistance (TEER). These changes were associated with decreased expression and disrupted localization of tight junction proteins occludin and claudin-3. The observed barrier dysfunction suggests that oral epithelial perturbation may represent an early toxicological response to PSNPs exposure. Pinoresinol pretreatment restored barrier integrity, normalizing TEER, FD4 permeability, and tight junction (TJ)-related protein expression. Mechanistically, PSNPs exposure suppressed CaMKKβ expression and AMPKα1 phosphorylation, whereas pinoresinol reactivated this pathway. Pharmacological inhibition of CaMKKβ with STO-609 attenuated the pinoresinol-mediated recovery of AMPKα1 phosphorylation and TJ-related protein expression, providing additional functional evidence for the involvement of CaMKKβ signaling in pinoresinol-mediated barrier protection. Molecular docking analysis suggested potential interactions between pinoresinol and CaMKKβ/AMPKα1, providing supportive structural context for these signaling effects. These findings indicate that PSNPs impair oral epithelial barrier function in association with disruption of TJ homeostasis and suppression of CaMKKβ-AMPKα1 signaling. Furthermore, the present study provides mechanistic insight into nanoplastic-associated epithelial barrier dysfunction and supports the potential of pinoresinol to attenuate PSNP-induced epithelial barrier impairment through modulation of CaMKKβ-AMPKα1 signaling.
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