Quercetin attenuates polystyrene nanoplastic-induced intestinal barrier injury through modulation of macrophage inflammatory responses
4 affiliations
- 1Guangdong Polytechnic of Science and Trade, Guangzhou, Guangdong, China
- 2National Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, Hubei, China
- 3Guangzhou Zoo and Guangzhou Wildlife Research Center, Guangzhou, Guangdong, China
- 4Guangdong Eco-engineering Polytechnic, Guangzhou, Guangdong, China
Abstract
Introduction: Polystyrene nanoplastics (PS-NPs) are emerging environmental contaminants that may impair intestinal barrier integrity, but the involvement of macrophage inflammatory responses remains incompletely understood. Quercetin is a natural flavonoid with well-established anti-inflammatory and immunomodulatory properties. This study investigated the role of macrophage inflammatory responses in PS-NP-induced intestinal injury and evaluated the protective effects of quercetin.
Methods: Male ICR mice were orally exposed to PS-NPs for 4 consecutive weeks, and the effects of quercetin intervention on colonic injury, inflammatory responses, tight junction-associated proteins, and macrophage polarization markers were evaluated. RAW 264.7 macrophages were used to further examine PS-NP-induced inflammatory responses and the effects of quercetin in vitro. An indirect Transwell co-culture system of RAW 264.7 macrophages and MODE-K intestinal epithelial cells was established to assess macrophage-mediated epithelial barrier alterations. NF-κB and STAT1 signaling activation was also examined.
Results: PS-NP exposure induced dose-dependent colonic histopathological injury, increased the expression of the pro-inflammatory cytokines IL-1β, TNF-α, and IL-6, and reduced the expression of the tight junction proteins ZO-1 and occludin. PS-NPs were also associated with a shift toward a pro-inflammatory macrophage phenotype, characterized by increased CD86 and decreased CD206 expression. Consistently, PS-NPs promoted inflammatory responses in RAW 264.7 macrophages and increased NF-κB p65 and STAT1 phosphorylation. In the Transwell co-culture system, MODE-K cells co-cultured with PS-NP-stimulated macrophages exhibited reduced tight junction-associated protein expression and disrupted junctional integrity. Quercetin treatment attenuated PS-NP-induced colonic injury and inflammatory responses, partially restored ZO-1 and occludin expression, modulated macrophage polarization-associated markers, and reduced NF-κB and STAT1 activation.
Discussion: These findings indicate that 50 nm PS-NP exposure induces intestinal inflammatory responses and barrier-associated injury accompanied by pro-inflammatory macrophage activation and altered NF-κB/STAT1 signaling. The co-culture findings further support the involvement of macrophage-derived inflammatory responses in epithelial barrier impairment. Quercetin attenuates PS-NP-induced intestinal injury, potentially in part through modulation of macrophage inflammatory responses accompanied by reduced NF-κB and STAT1 activation.
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BibTeX
@article{kang2026quercetin,
title = {{Quercetin attenuates polystyrene nanoplastic-induced intestinal barrier injury through modulation of macrophage inflammatory responses}},
author = {Jian Kang and Heng Yang and Yan Wang and Xin Zhang and Chunyang Zhu and Yanhong Zhou and Yanqin Li},
journal = {Frontiers in Pharmacology},
year = {2026},
month = oct,
doi = {10.3389/fphar.2026.1973458},
url = {https://doi.org/10.3389/fphar.2026.1973458},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Quercetin attenuates polystyrene nanoplastic-induced intestinal barrier injury through modulation of macrophage inflammatory responses
AU - Jian Kang
AU - Heng Yang
AU - Yan Wang
AU - Xin Zhang
AU - Chunyang Zhu
AU - Yanhong Zhou
AU - Yanqin Li
PY - 2026
DA - 2026/10/12
JO - Frontiers in Pharmacology
DO - 10.3389/fphar.2026.1973458
UR - https://doi.org/10.3389/fphar.2026.1973458
AB - Introduction: Polystyrene nanoplastics (PS-NPs) are emerging environmental contaminants that may impair intestinal barrier integrity, but the involvement of macrophage inflammatory responses remains incompletely understood. Quercetin is a natural flavonoid with well-established anti-inflammatory and immunomodulatory properties. This study investigated the role of macrophage inflammatory responses in PS-NP-induced intestinal injury and evaluated the protective effects of quercetin. Methods: Male ICR mice were orally exposed to PS-NPs for 4 consecutive weeks, and the effects of quercetin intervention on colonic injury, inflammatory responses, tight junction-associated proteins, and macrophage polarization markers were evaluated. RAW 264.7 macrophages were used to further examine PS-NP-induced inflammatory responses and the effects of quercetin in vitro. An indirect Transwell co-culture system of RAW 264.7 macrophages and MODE-K intestinal epithelial cells was established to assess macrophage-mediated epithelial barrier alterations. NF-κB and STAT1 signaling activation was also examined. Results: PS-NP exposure induced dose-dependent colonic histopathological injury, increased the expression of the pro-inflammatory cytokines IL-1β, TNF-α, and IL-6, and reduced the expression of the tight junction proteins ZO-1 and occludin. PS-NPs were also associated with a shift toward a pro-inflammatory macrophage phenotype, characterized by increased CD86 and decreased CD206 expression. Consistently, PS-NPs promoted inflammatory responses in RAW 264.7 macrophages and increased NF-κB p65 and STAT1 phosphorylation. In the Transwell co-culture system, MODE-K cells co-cultured with PS-NP-stimulated macrophages exhibited reduced tight junction-associated protein expression and disrupted junctional integrity. Quercetin treatment attenuated PS-NP-induced colonic injury and inflammatory responses, partially restored ZO-1 and occludin expression, modulated macrophage polarization-associated markers, and reduced NF-κB and STAT1 activation. Discussion: These findings indicate that 50 nm PS-NP exposure induces intestinal inflammatory responses and barrier-associated injury accompanied by pro-inflammatory macrophage activation and altered NF-κB/STAT1 signaling. The co-culture findings further support the involvement of macrophage-derived inflammatory responses in epithelial barrier impairment. Quercetin attenuates PS-NP-induced intestinal injury, potentially in part through modulation of macrophage inflammatory responses accompanied by reduced NF-κB and STAT1 activation.
SN - 1663-9812
ER -