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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Perfluorooctanesulfonic acid (PFOS), a fluorine-containing organic compound, can be widely detected in the environment and living organisms. Accumulating evidence has shown that PFOS breaks through different biological barriers resulting in cardiac toxicity, but the underlying molecular mechanisms remain unclear. Cannabidiol (CBD) is a nonpsychoactive cannabinoid without potential adverse cardiotoxicity and has antioxidant and anti-inflammatory properties that reduce multiorgan damage and dysfunction. For these reasons, the aim of this study was to research how PFOS caused heart injury and whether CBD could attenuate PFOS-induced heart injury. Mice were fed PFOS (5 mg/kg) and/or CBD (10 mg/kg) in vivo. In vitro, H9C2 cells were intervened with PFOS (200 μM) and/or CBD (10 μM). After PFOS exposure, oxidative stress levels and the mRNA and protein expression of apoptosis-related markers increased distinctly, accompanied by mitochondrial dynamic imbalance and energy metabolism disorders in mouse heart and H9C2 cells. Moreover, terminal deoxynucleotidyl transferase dUTP nick end labeling staining, acridine orange/ethidium bromide staining and Hoechst 33258 staining signaled that the number of apoptotic cells increased after exposure to PFOS. Noteworthy, CBD simultaneous treatment alleviated a series of damages caused by PFOS-mediated oxidative stress. Our results demonstrated that CBD could alleviate PFOS-induced mitochondrial dynamics imbalance and energy metabolism disorder causing cardiomyocyte apoptosis by improving the antioxidant capacity, suggesting that CBD may represent a novel cardioprotective strategy against PFOS-induced cardiotoxicity. Our findings facilitate the understanding of the cardiotoxic effects of PFOS and the important role of CBD in protecting cardiac health.

Nanoplastics (NPs) pollution poses a huge threat to the ecosystem and has become one of the environmental pollutants that have attracted much attention. There is increasing evidence that both oxidative stress and endoplasmic reticulum stress (ERS) are associated with polystyrene nanoplastics (PS‐NPs) exposure. Lipopolysaccharide (LPS) has been shown to induce apoptotic damage in various tissues, but whether PS‐NPs can aggravate LPS‐induced apoptosis in mouse kidneys through oxidative stress‐regulated inositol‐requiring enzyme 1 (IRE1)/X‐box binding protein 1 (XBP1) ERS pathway remains unclear. In this study, based on the establishment of in vitro and in vivo PS‐NPs and LPS exposure models alone and in combination in mice and HEK293 cells, the effects and mechanisms of PS‐NPs on LPS‐induced renal cell apoptosis were investigated. The results showed that PS‐NPs could aggravate LPS‐induced apoptosis. PS‐NPs/LPS can induce ERS through oxidative stress, activate the IRE1/XBP1 pathway, and promote the expression of apoptosis markers (Caspase‐3 and Caspase‐12). Kidney oxidative stress, ERS, and apoptosis in PS‐NPs + LPS combined exposure group were more severe than those in the single exposure group. Interestingly, 4‐phenylbutyric acid‐treated HEK293 cells inhibited the expression of the IRE1/XBP1 ERS pathway and apoptotic factors in the PS‐NPs + LPS combined exposure group. N‐acetyl‐L‐cysteine effectively blocked the activation of the IRE1/XBP1 ERS pathway, suggesting that PS‐NPs‐induced oxidative stress is an early event that triggers ERS. Collectively, these results confirmed that PS‐NPs aggravated LPS‐induced apoptosis through the oxidative stress‐induced IRE1/XBP1 ERS pathway. Our study provides new insights into the health threats of PS‐NPs exposed to mammals and humans.

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