# Sesamin Protects Against Polystyrene Microplastics-Induced Lung Injury via Attenuating Bcl2-Mediated Apoptosis

**Authors:** Yadong Zhang, Zhenao Zhang, Huanting Pei, Chongyue Zhang, Xiaolong Zhang, Simeng Qiao, Siqi Zhu, Ziyi Wang, Jingyi Ren, Yuxia Ma

PMC · DOI: 10.3390/antiox15030279 · Antioxidants · 2026-02-24

## TL;DR

Sesamin, a natural compound, protects against lung damage caused by microplastics by reducing cell death through the Bcl2 pathway.

## Contribution

This study identifies Bcl2 as a key target of sesamin in mitigating microplastic-induced lung injury.

## Key findings

- Sesamin reduces histopathological changes, inflammation, and oxidative stress in lung tissue caused by microplastics.
- Sesamin upregulates Bcl2 and downregulates Bax and Casp3, indicating anti-apoptotic effects.
- A Bcl2 inhibitor reduces the protective effects of sesamin, confirming its role in the mechanism.

## Abstract

Studies show microplastics (MPs) impair lung function directly and indirectly, yet effective solutions are lacking. In light of this, sesamin (Ses), a natural lignan-like compound with diverse pharmacological properties, may offer protection. The study aims to investigate whether Ses pretreatment can mitigate MPs-induced lung damage and to elucidate the underlying mechanisms. Male C57BL/6 mice received MPs (10,000 μg/L) in drinking water, with varying Ses doses gavaged daily for 28 days. Computational pharmacology and in vivo/in vitro experiments, including histology, immunofluorescence, and western blot, were used to elucidate Ses’s protective mechanisms. In vivo experiments showed Ses can alleviate MPs-induced histopathological alterations, inflammatory responses, and oxidative stress in lung tissue. Computational pharmacology suggested that the protective mechanism of Ses may be associated with the apoptotic signaling pathway, with Bcl2 as its potential target. Both in vivo and in vitro studies demonstrated that Ses significantly upregulates Bcl2 expression while downregulating Bax and Casp3. Notably, a Bcl2 inhibitor substantially attenuated Ses’s protective effects. Our research suggests that Ses can mitigate MPs-induced lung injury by modulating the apoptotic signaling pathway, with Bcl2 identified as a key target. Dietary supplementation may represent a promising intervention strategy for preventing and managing food safety risks associated with MPs.

## Linked entities

- **Genes:** BCL2 (BCL2 apoptosis regulator) [NCBI Gene 596], BAX (BCL2 associated X, apoptosis regulator) [NCBI Gene 581], CASP3 (caspase 3) [NCBI Gene 836]
- **Chemicals:** sesamin (PubChem CID 5204)

## Full-text entities

- **Genes:** Bax (BCL2-associated X protein) [NCBI Gene 12028], Bcl2 (B cell leukemia/lymphoma 2) [NCBI Gene 12043] {aka Bcl-2, C430015F12Rik, D630044D05Rik, D830018M01Rik}, Casp3 (caspase 3) [NCBI Gene 12367] {aka A830040C14Rik, AC-3, CASP-3, CC3, CPP-32, CPP32}
- **Diseases:** inflammatory (MESH:D007249), Lung Injury (MESH:D055370), lung damage (MESH:D008171)
- **Chemicals:** lignan (MESH:D017705), Ses (MESH:C054125), Polystyrene (MESH:D011137)
- **Species:** Mus musculus (house mouse, species) [taxon 10090]

## Full text

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## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13023509/full.md

## References

53 references — full list in the complete paper: https://tomesphere.com/paper/PMC13023509/full.md

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Source: https://tomesphere.com/paper/PMC13023509