Selenium-deficient diet induces inflammatory response in the pig adrenal glands by activating TLR4/NF-κB pathway via miR-30d-R_1.

Selenium (Se) is an important trace element to maintain the body's dynamic balance. Lack of Se can cause inflammation. Studies have shown that inflammation often leads to disorders of the hypothalamic-pituitary-adrenal axis, but the mechanism by which Se deficiency causes inflammation of the porcine adrenal glands is still unclear. In order to study the effect of Se deficiency on the adrenal glands of pigs, we obtained Se-deficient pig adrenal glands through a low-Se diet. The results of mass spectrometry showed that the Se content in the Se-deficient group was only one-tenth of the control group. We detected the expression of the toll-like receptor 4 (TLR4) and downstream factors by qRT-PCR and Western blotting, and found that the lack of Se affected the TLR4/NF-κB pathway. It is known that miR-155-3p, miR-30d-R_1, and miR-146b have all been verified for targeting relationship with TLR4. We confirmed by qRT-PCR that miR-30d-R_1 decreased most significantly in the Se-deficient pig model. Then we tested 25 selenoproteins and some indicators of oxidative stress. It is confirmed that Se deficiency reduces the antioxidant capacity and induces oxidative stress in pig adrenal tissue. In short, a diet lacking Se induces oxidative stress in pig adrenal tissues and leads to inflammation through the miR-30d-R_1/TLR4 pathway. This study provides a reference for the prevention of adrenal inflammation in pigs from a nutritional point of view.

Methionine selenium antagonizes LPS-induced necroptosis in the chicken liver via the miR-155/TRAF3/MAPK axis.

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.