Related Experiment Video
Updated: Sep 7, 2025

Using Chicken Embryo as a Powerful Tool in Assessment of Developmental Cardiotoxicities
Published on: March 21, 2021
Polystyrene microplastics-induced cardiotoxicity in chickens via the ROS-driven NF-κB-NLRP3-GSDMD and AMPK-PGC-1α
Yue Zhang1, Kai Yin1, Dongxu Wang1
1College of Wildlife and Protected Area, Northeast Forestry University, Harbin 150040, Heilongjiang, PR China.
Abstract:
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.
Insights
Polystyrene microplastics (PS-MPs) cause significant heart damage in chickens by inducing pyroptosis, inflammation, and mitochondrial dysfunction via the NF-κB-NLRP3-GSDMD and AMPK-PGC-1α pathways. N-acetylcysteine (NAC) showed protective effects in vitro.
Area of Science:
- Environmental Toxicology
- Cardiovascular Pathology
- Cellular Biology
Background:
- Microplastic (MP) pollution is a growing environmental concern with largely unknown health impacts.
- The specific mechanisms by which MPs induce cardiac injury in poultry remain unclear.
Purpose of the Study:
- To investigate the effects of polystyrene microplastics (PS-MPs) on chicken hearts and cardiomyocytes.
- To elucidate the molecular pathways involved in PS-MP-induced cardiac damage.
Main Methods:
- Exposure of chickens and primary cardiomyocytes to varying concentrations of 5 μm PS-MPs.
- Histopathological examination, ultrastructural analysis, and molecular assays to assess cardiac injury.
- Investigation of key signaling pathways including NF-κB-NLRP3-GSDMD and AMPK-PGC-1α.
Main Results:
- PS-MPs induced severe cardiac pathological damage, ultrastructural changes, myocardial pyroptosis, inflammation, and mitochondrial lesions.
- PS-MPs led to oxidative stress, ROS overproduction, and dysregulated antioxidant enzymes.
- Molecular analysis revealed PS-MP-induced activation of the NF-κB-NLRP3-GSDMD pathway and inhibition of the AMPK-PGC-1α pathway, leading to mitochondrial and energy metabolism dysfunction.
- N-acetylcysteine (NAC) demonstrated a protective effect against these PS-MP-induced damages in vitro.
Conclusions:
- PS-MPs trigger cardiac injury in chickens through oxidative stress, ROS overload, and subsequent activation of pyroptosis and inflammatory pathways.
- Mitochondrial damage and energy metabolism disorders are key consequences of PS-MP exposure, mediated by the NF-κB-NLRP3-GSDMD and AMPK-PGC-1α signaling.
- These findings provide a mechanistic basis for understanding and mitigating microplastic toxicity in poultry.

