Abstract：
In recent years, the study of microplastics (MPs) and nanoplastics (NPs) and their effects on human health has gained significant attention. The impacts of NPs on lipid metabolism and the specific mechanisms involved remain poorly understood. To address this, we utilized high-throughput sequencing and molecular biology techniques to investigate how endoplasmic reticulum (ER) stress might affect hepatic lipid metabolism in the presence of polystyrene nanoplastics (PS-NPs). Our findings suggest that PS-NPs activate the PERK-ATF4 signaling pathway, which in turn upregulates the expression of genes related to lipid synthesis via the ATF4-PPARγ/SREBP-1 pathway. This activation leads to an abnormal accumulation of lipid droplets in the liver. 4-PBA, a known ER stress inhibitor, was found to mitigate the PS-NPs-induced lipid metabolism disorder. These results demonstrate the hepatotoxic effects of PS-NPs and clarify the mechanisms of abnormal lipid metabolism induced by PS-NPs.
摘要：
近年来,微塑料(MPs)和纳米塑料(NPs)及其对人体健康影响的研究得到了广泛的关注。NPs对脂质代谢的影响和所涉及的具体机制仍然知之甚少。为了解决这个问题，我们利用高通量测序和分子生物学技术研究了在聚苯乙烯纳米塑料(PS-NP)存在下内质网(ER)应激如何影响肝脂质代谢.我们的研究结果表明，PS-NP激活PERK-ATF4信号通路，进而通过ATF4-PPARγ/SREBP-1途径上调与脂质合成相关的基因的表达。这种激活导致脂滴在肝脏中的异常积累。4-PBA,一种已知的ER应激抑制剂，被发现可减轻PS-NP诱导的脂质代谢紊乱。这些结果证明了PS-NP的肝毒性作用，并阐明了PS-NP诱导的异常脂质代谢的机制。
