Microplastics are a growing concern as pollutants that impact both public health and the environment. However, the toxic effects of polypropylene microplastics (PP‐MPs) are not well understood. This study aimed to investigate the effects of PP‐MPs on cardiotoxicity and its underlying mechanisms. The cardiotoxicity of exposure to different amounts of PP‐MPs were investigated in both ICR mice and H9C2 cells. Our results demonstrated that sub‐chronic exposure to 5 and 50 mg/L PP‐MPs led to myocardial structural damage, apoptosis, and fibrosis in mice cardiomyocytes. Flow cytometry analysis revealed that PP‐MPs could decrease mitochondrial membrane potential and induce apoptosis in H9C2 cells. Western blotting revealed decreased expression of Bcl‐2, poly(ADP‐ribose) polymerase (PARP) and caspase 3 and increased expression of Bax, cleaved‐PARP, and cleaved‐caspase 3 in PP‐MPs‐treated cardiac tissue and H9C2 cells. These results confirmed the apoptotic effects induced by PP‐MPs. Moreover, PP‐MPs treatment triggered oxidative stress, as evidenced by the increased levels of malondialdehyde; reduction in glutathione peroxidase, superoxide dismutase, and catalase activities in mice cardiac tissues; and increased reactive oxygen species levels in H9C2 cells. Finally, western blotting demonstrated that exposure to PP‐MPs significantly reduced the expression levels of Nrf2 and p‐ERK proteins associated with MAPK‐Nrf2 pathway in both cardiac tissue and H9C2 cells. Overall, our findings indicate that PP‐MPs can induce cardiomyocyte apoptosis through MAPK‐Nrf2 signaling pathway, which is triggered by oxidative stress. This study provides a foundation for determining the effects of PP‐MPs on cardiotoxicity and their underlying mechanisms.

中文翻译：

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暴露于聚丙烯微塑料会通过氧化应激和 MAPK-Nrf2 信号通路激活导致心肌细胞凋亡


微塑料作为影响公众健康和环境的污染物，越来越受到关注。然而，聚丙烯微塑料 （PP-MP） 的毒性作用尚不清楚。本研究旨在探讨 PP-MPs 对心脏毒性的影响及其潜在机制。在 ICR 小鼠和 H9C2 细胞中研究了暴露于不同量 PP-MPs 的心脏毒性。我们的结果表明，亚慢性暴露于 5 和 50 mg/L PP-MPs 会导致小鼠心肌细胞发生心肌结构损伤、细胞凋亡和纤维化。流式细胞术分析显示，PP-MPs 可降低线粒体膜电位并诱导 H9C2 细胞凋亡。Western blotting 显示 PP-MPs 处理的心脏组织和 H9C2 细胞中 Bcl-2 、聚 （ADP-核糖） 聚合酶 （PARP） 和 caspase 3 的表达降低，Bax、裂解-PARP 和裂解-caspase 3 的表达增加。这些结果证实了 PP-MPs 诱导的凋亡作用。此外，PP-MPs 处理触发了氧化应激，丙二醛水平升高证明了这一点;降低小鼠心脏组织中谷胱甘肽过氧化物酶、超氧化物歧化酶和过氧化氢酶活性;以及 H9C2 细胞中的活性氧水平增加。最后，蛋白质印迹表明，暴露于 PP-MPs 可显著降低心脏组织和 H9C2 细胞中与 MAPK-Nrf2 通路相关的 Nrf2 和 p-ERK 蛋白的表达水平。总体而言，我们的研究结果表明，PP-MPs 可以通过氧化应激触发的 MAPK-Nrf2 信号通路诱导心肌细胞凋亡。本研究为确定 PP-MPs 对心脏毒性的影响及其潜在机制提供了基础。