Polystyrene nanoplastics potentiate the development of hepatic fibrosis in high fat diet fed mice

Li, Ling; Xu, Minjie; He, Chao; Wang, Hui; Hu, Qinglian

doi:10.1002/tox.23404

Cited by 49 publications

(18 citation statements)

References 55 publications

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“…Microplastics (MPs) and nanoplastics (NPs) wastes pollution has led to an alarming situation, and subsequent the ecological environment and human health problems have gradually attracted social attention 1,2 . Compared to MPs, NPs, as particles with a particle size of 1–100 nm, more easily enter aquatic species and other animals including humans through the food chain 3 .…”

Section: Introductionmentioning

confidence: 99%

Polystyrene nanoplastics exacerbated lipopolysaccharide‐induced necroptosis and inflammation via the ROS/MAPK pathway in mice spleen

Tang

Fan

et al. 2022

Environmental Toxicology

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Plastics are novel environmental pollutants with potential threats to the ecosystem. At least 5.25 trillion plastic particles in the environment, of which nanoplastics are <100 nm in diameter. Polystyrene nanoplastics (PS‐NPs) exposure damaged the spleen's immune function. Lipopolysaccharide (LPS) induced other toxicants to damage cells and organs, triggering inflammation. However, the mechanism of PS‐NPs aggravated LPS‐induced spleen injury remains unclear. In this study, the PS‐NPs or/and LPS mice exposure model was replicated by intraperitoneal injection of PS‐NPs or/and LPS, and PS‐NPs or/and LPS were exposed to RAW264.7 cells. The histopathological and ultrastructural changes of the mice spleen were observed by H&E staining and transmission electron microscope. Western Blot, qRT‐PCR, and fluorescent probes staining were used to detect reactive oxygen species (ROS), oxidative stress indicators, inflammatory factors, and necroptosis‐related indicators in mice spleen and RAW264.7 cells. The results showed that PS‐NPs or LPS induced oxidative stress, activated the MAPK pathway, and eventually caused necroptosis and inflammation in mice spleen and RAW264.7 cells. Compared with the single treatment group, the changes in PS‐NPs + LPS group were more obvious. Furthermore, ROS inhibitor N‐Acetyl‐L‐cysteine (NAC) significantly inhibited the activation of the mitogen‐activated protein kinase (MAPK) signaling pathway caused by co‐treatment of PS‐NPs and LPS, reducing necroptosis and inflammation. The results demonstrated that PS‐NPs promoted LPS‐induced spleen necroptosis and inflammation in mice through the ROS/MAPK pathway. This study increases the data on the damage of PS‐NPs to the organism and expands the research ideas and clues.

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Section: Introductionmentioning

confidence: 99%

Polystyrene nanoplastics exacerbated lipopolysaccharide‐induced necroptosis and inflammation via the ROS/MAPK pathway in mice spleen

Tang

Fan

et al. 2022

Environmental Toxicology

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“…9,10 Compelling evidence shows that ingested PS-MPs lead to various aspects of tissue or organ dysfunction in vitro and vivo. 11,12 PS-MPs first enter the gastrointestinal tract, and these particles could subsequently be transferred to tissue areas by cell internalization or blood circulation. 13 The mice were taken PS-MPs, resulting in intestinal dysregulation, inflammation, and disturbed liver metabolism.…”

mentioning

confidence: 99%

Polystyrene microplastics induce autophagy and apoptosis in birds lungs via PTEN/PI3K/AKT/mTOR

Yin

et al. 2022

Environmental Toxicology

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Microplastics (MPs) seriously pollute and potentially threaten human health. Birds are sentinels of environmental pollutants, which respond quickly to contamination events and reveal current environmental exposure. Therefore, birds are good bioindicators for monitoring environmental pollutants. However, the mechanism of lung injury in birds and the role of the PTEN/PI3K/AKT axis are unknown. In this study, broilers treated with different polystyrene microplastics (PS‐MPs) (0, 1, 10, and 100 mg/L) were exposed to drinking water for 6 weeks to analyze the effect of PS‐MPs on lung injury of broilers. The results showed that with the increase of PS‐MPs concentration, malonaldehyde (MDA) content increased, and catalase (CAT) and glutathione (GSH) activity decreased, further leading to oxidative stress. PS‐MPs caused the PI3K/Akt/mTOR pathway to be inhibited by phosphorylation, and autophagy accelerated formation (LC3) and degradation (p62), causing autophagy. In PS‐MPs exposed lung tissues, the expression of Bax/Bcl‐2 and Caspase family increased, and MAPK signaling pathways (p38, ERK, and JNK) showed an increase in phosphorylation level, thus leading to cell apoptosis. Our research showed that PS‐MPs could activate the antioxidant system. The antioxidant system unbalance‐regulated Caspase family, and PTEN/PI3K/AKT pathways initiated apoptosis and autophagy, which in turn led to lung tissue damage in chickens. These results are of great significance to the toxicological study of PS‐MPs and the protection of the ecosystem.

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“…Histological changes were investigated using a light microscope (Leica DM300, Wetzlar, Germany) under 200x magnification. The inflammation score of hepatic lobules was determined by counting the inflammatory lesions under a microscope at ×20 magnification as follows: 0 points for no lesions, 1 point for <2 lesions, 2 points for 2–4 lesions, and 3 points for >4 lesions ( Li et al, 2022 ). The data were collected by an investigator who was blinded to the origin of the tissue sections.…”

Section: Methodsmentioning

confidence: 99%

Acute Endoplasmic Reticulum Stress Induces Inflammation Reaction, Complement System Activation, and Lipid Metabolism Disorder of Piglet Livers: A Proteomic Approach

et al. 2022

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Endoplasmic reticulum stress (ERS) is closely associated with the occurrence and development of many liver diseases. ERS models mostly include experimental animals such as rats and mice. However, pigs are more similar to humans with regards to digestion and metabolism, especially liver construction, yet few reports on ERS in pigs exist. In order to explore changes in the liver under ERS, we used tunicamycin (TM), which can cause liver jaundice and damage liver function, to establish acute ERS models in piglets using a low TM dosage (LD, 0.1 mg/kg body weight (bw)), high TM dosage (HD, 0.3 mg/kg bw), or vehicle for 48 h. We found that both LD- and HD-induced ERS, as verified by the ERS-linked proteins. Furthermore, the concentrations of the proinflammatory cytokines, namely, TNF-α and IL-6 were elevated in TM-treated piglet livers, and the plasma levels of IL-6 and CRP were also higher, indicating the occurrence of inflammation in TM-treated piglets. The complement system was activated in TM-treated piglets, as indicated by increased levels of complement factors and activation products C3, C5a, and AP50. In order to gain insights into the global changes in liver proteins under ERS, we performed an isobaric tag for relative and absolute quantitation (iTRAQ)-based proteomic analysis on the livers of HD- and vehicle-treated piglets. Proteomic analysis identified 311 differentially expressed proteins (DEPs) between the two groups, and a Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis suggested that the DEPs were mainly enriched in signaling pathways such as metabolic pathways, protein processing in the endoplasmic reticulum, and complement and coagulation cascades. Many proteins involved in protein folding, lipid transport, and oxidation were upregulated. Proteins involved in lipid synthesis were downregulated to alleviate liver steatosis, and most complement factors were upregulated to protect the body, and Pearson correlation analysis found that most of the DEPs in the complement and coagulation pathway were significantly correlated with plasma CRP, IL6 and AP50. Our results revealed that TM can activate ERS, marked by liver injury and steatosis, inflammatory reactions, and complement activation in piglets.

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Polystyrene nanoplastics potentiate the development of hepatic fibrosis in high fat diet fed mice

Cited by 49 publications

References 55 publications

Polystyrene nanoplastics exacerbated lipopolysaccharide‐induced necroptosis and inflammation via the ROS/MAPK pathway in mice spleen

Polystyrene nanoplastics exacerbated lipopolysaccharide‐induced necroptosis and inflammation via the ROS/MAPK pathway in mice spleen

Polystyrene microplastics induce autophagy and apoptosis in birds lungs via PTEN/PI3K/AKT/mTOR

Acute Endoplasmic Reticulum Stress Induces Inflammation Reaction, Complement System Activation, and Lipid Metabolism Disorder of Piglet Livers: A Proteomic Approach

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