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

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Mice drank water containing polystyrene microplastics for 28 days, and some also received sesamin, a compound from sesame seeds. The sesamin groups showed less lung inflammation, oxidative stress and tissue change. Cell and mouse experiments pointed to Bcl2, a protein that regulates cell death, as the likely target.

Polymers
Models
Study Type In vivo

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.

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