The extensive existing of microplastics (MPs) in the ecosystem have increased considerable attention concerning their potential adverse effects, the toxicities and the underlying mechanism of MPs are still scarce. To explore the effect of MPs on cardiac tissue in Wistar rats and unravel the mechanism of pyroptosis and oxidative stress in the process of cardiomyocytes injury, 32 male Wister rats were divided into control group and three model groups, which were exposed to 0.5 mm PS MPs at 0.5, 5 and 50 mg/L for 90 days. Results revealed that MPs could damage cardiac structure and function with impaired mitochondria integrity, as well as increased levels of creatine kinase-MB and cardiac troponinI (cTnI). Moreover, MPs administration triggered oxidative stress as indicated by increased levels of malondialdehyde and decreased activity of superoxide dismutase, glutathione peroxidase and catalase. Treatment with MPs resulted in apoptosis and pyroptosis as evidenced by increasing expressions of interleukin (IL)-1β, IL-18. Additionally, MPs were shown to induce the NOD-like receptor protein 3 inflammasomes activation in cardiac tissue, enabling activation of Caspase-1-dependent signaling pathway induced by inflammatory stimuli resulting from oxidative stress. In summary, these results illustrated that pyroptosis played a vital role in polystyrene MPs-induced cardiotoxicity, which might be helpful to understand the mechanism of cardiac dysfunction and induced by MPs.

中文翻译：

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聚苯乙烯微塑料通过NLRP3/Caspase-1信号通路和氧化应激对Wistar大鼠心肌细胞焦亡的影响

微塑料（MPs）在生态系统中的广泛存在引起了人们对其潜在不利影响的广泛关注，MPs的毒性和潜在机制仍然很少。为探讨 MPs 对 Wistar 大鼠心脏组织的影响，揭示心肌细胞损伤过程中细胞焦亡和氧化应激的机制，将 32 只雄性 Wister 大鼠分为对照组和 3 个模型组，分别暴露于 0.5 mm PS MPs在 0.5、5 和 50 mg/L 下持续 90 天。结果表明，MPs 会损害心脏结构和功能，损害线粒体完整性，以及增加肌酸激酶-MB 和心肌肌钙蛋白 I (cTnI) 的水平。而且，MPs 给药引发氧化应激，表现为丙二醛水平升高和超氧化物歧化酶、谷胱甘肽过氧化物酶和过氧化氢酶活性降低。MPs 处理导致细胞凋亡和细胞焦亡，白细胞介素 (IL)-1β、IL-18 的表达增加证明了这一点。此外，MPs 可诱导心脏组织中 NOD 样受体蛋白 3 炎症小体激活，从而激活由氧化应激引起的炎症刺激诱导的 Caspase-1 依赖性信号通路。总之，这些结果表明细胞焦亡在聚苯乙烯 MPs 诱导的心脏毒性中起重要作用，这可能有助于理解 MPs 诱导的心脏功能障碍的机制。MPs 处理导致细胞凋亡和细胞焦亡，白细胞介素 (IL)-1β、IL-18 的表达增加证明了这一点。此外，MPs 可诱导心脏组织中 NOD 样受体蛋白 3 炎症小体激活，从而激活由氧化应激引起的炎症刺激诱导的 Caspase-1 依赖性信号通路。总之，这些结果表明细胞焦亡在聚苯乙烯 MPs 诱导的心脏毒性中起重要作用，这可能有助于理解 MPs 诱导的心脏功能障碍的机制。MPs 处理导致细胞凋亡和细胞焦亡，白细胞介素 (IL)-1β、IL-18 的表达增加证明了这一点。此外，MPs 可诱导心脏组织中 NOD 样受体蛋白 3 炎症小体激活，从而激活由氧化应激引起的炎症刺激诱导的 Caspase-1 依赖性信号通路。总之，这些结果表明细胞焦亡在聚苯乙烯 MPs 诱导的心脏毒性中起重要作用，这可能有助于理解 MPs 诱导的心脏功能障碍的机制。激活由氧化应激引起的炎症刺激诱导的 Caspase-1 依赖性信号通路。总之，这些结果表明细胞焦亡在聚苯乙烯 MPs 诱导的心脏毒性中起重要作用，这可能有助于理解 MPs 诱导的心脏功能障碍的机制。激活由氧化应激引起的炎症刺激诱导的 Caspase-1 依赖性信号通路。总之，这些结果表明细胞焦亡在聚苯乙烯 MPs 诱导的心脏毒性中起重要作用，这可能有助于理解 MPs 诱导的心脏功能障碍的机制。