The yellow line displays the promotion and the green line displays the inhibition. miR: microRNA; Se: selenium.

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Neutrophil extracellular traps (NETs) are reticular structures formed by myeloperoxidase (MPO), histones, and neutrophil elastase (NE) that are released from neutrophils in response to pathogenic stimuli. Chlorpyrifos (CPF) is wildly used as an organophosphorus pesticide that causes a range of toxicological and environmental problems. Exposure to CPF can increase the production of neutrophils in carps, and this increase can be considered a biomarker of water pollution. To explore a relationship between NETs and CPF and its mechanism of influence, we treated neutrophils from the blood of carp with 1 μg/mL phorbol 12-myristate 13-acetate (PMA), 0.325 mg/L CPF, or 20 μM necrostatin-1 (Nec-1). The production of MPO and NETs was reduced in the CPF+PMA group compared with that in the PMA group. CPF can cause an increase in reactive oxygen species (ROS), while inhibiting respiratory burst caused by PMA stimulation. We found that the expression levels of protein-coupled receptor 84 (gpr84), dystroglycan (DAG), proto-oncogene serine/threonine kinase (RAF), protein kinase C (PKC), and mitogen-activated protein kinase 3 (MAPK3) in the CPF+PMA group were lower than those in the PMA group, indicating that the PKC-MAPK pathway was suppressed. The expression levels of cylindromatosis (CYLD), mixed lineage kinase domain-like pseudokinase (MLKL), receptor-interacting serine-threonine kinase 1 (RIP1), and receptor-interacting serine-threonine kinase 3 (RIP3) were increased, and the expression levels of caspase 8 were reduced by CPF, indicating that CPF may cause necroptosis. The addition of Nec-1 restored the number of NETs in the CPF+PMA group. The results indicate that CPF reduced the production of NETs by inhibiting respiratory burst and increasing necroptosis. The results contribute to the understanding of the immunotoxicological mechanism of CPF and provide a reference for comparative medical studies.

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Organic selenium has antioxidation and disease treatment effects. To explore the mechanisms of how methionine selenium alleviates necroptosis in the liver and whether this process is related to microRNA (miRNA) and the mitogen‐activated protein kinase (MAPK) pathway, an animal model of methionine selenium and the lipopolysaccharide (LPS) interaction was established. The morphology, inflammatory factor (tumor necrosis factor‐α [TNF‐α]), necroptosis‐related genes (RIP1, RIP3, MLKL, and caspase 8), MAPK pathway‐related genes (JNK, ERK, and p38, p‐JNK, p‐ERK, and p‐p38), gga‐miR‐155, TRAF3 (predicted target of gga‐miR‐155), and oxidative stress‐related indicators (SOD, MDA, CAT, GSH, and GSH‐Px) were analyzed from the perspective of the miR‐155/TRAF3/MAPK axis to elucidate the mechanism of methionine selenium on the LPS‐induced necroptosis mechanism in the chicken liver. The current results suggested that methionine selenium antagonizes oxidative stress, inflammation, and the MAPK pathway, thereby antagonizing the occurrence of necroptosis through multiple mechanisms. At the same time, methionine selenium affects miR‐155/TRAF3/MAPK signaling, reduces miR‐155 expression, and upregulates TRAF3 expression to inhibit necroptosis. This information provided new ideas and a theoretical basis for the practical application of methionine selenium, and it also enriched the study of miRNAs in birds and provided a reference for comparative medicine.