College of Wildlife and Protected Area, Northeast Forestry University, Harbin 150040, Heilongjiang, PR China.
College of Wildlife and Protected Area, Northeast Forestry University, Harbin 150040, Heilongjiang, PR China.
Sci Total Environ. 2022 Sep 20;840:156727. doi: 10.1016/j.scitotenv.2022.156727. Epub 2022 Jun 14.
Microplastics (MPs) pollution is getting increasingly prominent, and its dangers have attracted widespread attention. The heart is the central hub of the organism's survival, and the mechanism of MPs-induced heart injury in chickens is unknown. Here, we investigated the effects of 5 μm polystyrene microplastics (PS-MPs) on the heart and primary cardiomyocytes of chickens at varied concentrations. We observed that PS-MPs caused severe pathological damage and ultrastructural changes in heart, induced myocardial pyroptosis, inflammatory cell infiltration and mitochondrial lesions. PS-MPs evoked abnormal antioxidant enzyme content and ROS overproduction. Detailed mechanistic investigation indicated that PS-MPs triggered pyroptosis via NF-κB-NLRP3-GSDMD axis and exacerbated myocardial inflammation (NLRP3, Caspase-1, IL-1β, IL-18, ASC, GSDMD, NF-κB, COX-2, iNOS and IL-6 overexpression). Additionally, PS-MPs induced mitochondrial damage (TFAM, OPA1, MFN1 and MFN2 down-expression, DRP1 and Fis1 overexpression) and energy metabolism disorders (HK2, PKM2, PDHX and LDH up-regulation) by inhibiting AMPK-PGC-1α pathway. Interestingly, NAC alleviated these aberrant manifestations in vitro. We suggested that PS-MPs driven alterations in NF-κB-NLRP3-GSDMD and AMPK-PGC-1α pathways via ROS overload, which in turn triggered oxidative stress, myocardial pyroptosis, inflammation, mitochondrial and energy metabolism dysfunction. This provided theoretical bases for protecting chickens from toxic injury by MPs.
微塑料（MPs）污染日益突出，其危害已引起广泛关注。心脏是机体生存的中心枢纽，MPs 诱导鸡心脏损伤的机制尚不清楚。在这里，我们研究了不同浓度的 5μm 聚苯乙烯微塑料（PS-MPs）对鸡心脏和原代心肌细胞的影响。我们观察到 PS-MPs 导致心脏严重的病理损伤和超微结构改变，诱导心肌细胞焦亡、炎症细胞浸润和线粒体损伤。PS-MPs 引起抗氧化酶含量异常和 ROS 过度产生。详细的机制研究表明，PS-MPs 通过 NF-κB-NLRP3-GSDMD 轴引发焦亡，并加剧心肌炎症（NLRP3、Caspase-1、IL-1β、IL-18、ASC、GSDMD、NF-κB、COX-2、iNOS 和 IL-6 过表达）。此外，PS-MPs 通过抑制 AMPK-PGC-1α 通路诱导线粒体损伤（TFAM、OPA1、MFN1 和 MFN2 表达下调，DRP1 和 Fis1 过表达）和能量代谢障碍（HK2、PKM2、PDHX 和 LDH 上调）。有趣的是，NAC 在体外减轻了这些异常表现。我们认为，PS-MPs 通过 ROS 过载驱动 NF-κB-NLRP3-GSDMD 和 AMPK-PGC-1α 通路的改变，进而引发氧化应激、心肌焦亡、炎症、线粒体和能量代谢功能障碍。这为保护鸡免受 MPs 的毒性损伤提供了理论依据。
