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.
Both bisphenol A (BPA) and selenium (Se) deficiency can affect the expression of microRNAs (miRNAs), which can specifically regulate its target mRNA and induce apoptosis, and play a significant role in cardiovascular injury diseases. To explore the mechanism of apoptosis induced by BPA and Se deficiency in chicken arterial endothelial tissue and the role of miRNAs in this process, the model of BPA exposure/Se deficiency in chicken and PAEC cells have been employed. The targeting relationship between miR‐215‐3p and iodothyronine deiodinase 1 (Dio1) in PAEC was verified by double luciferase gene report. The level of miR‐215‐3p was detected by qRT‐PCR. The oxidative stress level of arterial endothelial cells was detected by oxidative stress kit and DCFH‐DA probe method. The PI3K/AKT pathway, mitochondrial dynamics, and apoptosis‐related genes were detected by qRT‐PCR and western blot. The mitochondrial ATP level and nitric oxide synthases (NOSs) level were detected with the kit. TUNEL, acridine orange/ethidium bromide, and flow cytometry were used to detect the level of apoptosis. The results showed that BPA exposure and Se deficiency led to overexpression of miR‐215‐3p, aggravated oxidative stress, inhibited activation of PI3K/AKT pathway, promoted mitochondrial division, increased expression of apoptosis related genes, and finally led to apoptosis of chicken arterial endothelial cells. We also established knockdown/overexpression models of miR‐215‐3p and Dio1 in vitro, and found that overexpression of miR‐215‐3p and knockout of Dio1 can induce apoptosis. Interestingly, miR‐215‐3p‐Inhibitor and N‐acetyl‐
l‐cysteine (NAC) partially prevented apoptosis caused by BPA exposure and Se deficiency, and LY294002 aggravated apoptosis. These results suggest that BPA exposure aggravates the apoptosis of Se deficient arterial endothelial cells in chickens by regulating the ROS/PI3K/AKT pathway activated by miR‐215‐3p/Dio1. The miR‐215‐3p/Dio1 axis provides a new way to understand the toxic mechanism of BPA exposure and Se deficiency, and reveals a new regulatory model of apoptosis damage in vascular diseases.
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