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聚苯乙烯微塑料通过激活 Wnt/β-连环蛋白信号通路并促进大鼠心肌细胞凋亡引起心脏纤维化。

Polystyrene microplastics cause cardiac fibrosis by activating Wnt/β-catenin signaling pathway and promoting cardiomyocyte apoptosis in rats.

机构信息

College of Clinical Medicine, Bin Zhou Medical University, Yan Tai, PR China.

Key Laboratory of Cardiovascular Epidemiology & Department of Epidemiology, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.

出版信息

Environ Pollut. 2020 Oct;265(Pt A):115025. doi: 10.1016/j.envpol.2020.115025. Epub 2020 Jun 18.

DOI:10.1016/j.envpol.2020.115025
PMID:32806417
Abstract

Microplastics (MPs) are new persistent organic pollutants derived from the degradation of plastics. They can accumulate along the food chain and enter the human body through oral administration, inhalation and dermal exposure. To identify the impact of Polystyrene (PS) MPs on the cardiovascular system and the underlying toxicological mechanism, 32 male Wister rats were divided into control group and three model groups, which were exposed to 0.5 μm PS MPs at 0.5, 5 and 50 mg/L for 90 days. Our results suggested that PS MPs exposure increased Troponin I and creatine kinase-MB (CK-MB) levels in serum, resulted in structure damage and apoptosis of myocardium, and led to collagen proliferation of heart. Moreover, PS MPs could induce oxidative stress and thus activate fibrosis-related Wnt/β-catenin signaling pathway. These results suggested that PS MPs could lead to cardiovascular toxicity by inducing cardiac fibrosis via activating Wnt/β-catenin pathway and myocardium apoptosis triggered by oxidative stress. The present study provided some novelty evidence to elucidate the potential mechanism of cardiovascular toxicity induced by PS MPs.

摘要

微塑料(MPs)是源自塑料降解的新型持久性有机污染物。它们可以沿着食物链积累,并通过口服、吸入和皮肤暴露进入人体。为了确定聚苯乙烯(PS) MPs 对心血管系统的影响及其潜在的毒理学机制,将 32 只雄性 Wister 大鼠分为对照组和三个模型组,分别在 0.5μm PS MPs 浓度为 0.5、5 和 50mg/L 下暴露 90 天。我们的结果表明,PS MPs 暴露会增加血清中心肌肌钙蛋白 I 和肌酸激酶同工酶-MB(CK-MB)的水平,导致心肌结构损伤和凋亡,并导致心脏胶原增殖。此外,PS MPs 可诱导氧化应激,从而激活纤维化相关的 Wnt/β-连环蛋白信号通路。这些结果表明,PS MPs 可通过激活 Wnt/β-连环蛋白通路和氧化应激引发的心肌细胞凋亡导致心脏纤维化,从而导致心血管毒性。本研究为阐明 PS MPs 引起心血管毒性的潜在机制提供了一些新颖的证据。

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