The mechanism of p38 MAPK, NF-κB, and IL-6 in T-2 toxin and/or selenium deficiency induced spleen injury.

Both T-2 toxin and selenium (Se) cause immune impairment in the spleen, but the mechanism of their occurrence is not clear. In this experiment, the Se content of the spleen was tested by atomic fluorescence spectrometry after a 12-week intervention in Sprague-Dawley (SD) rats, divided into normal, normal + T-2 toxin (10 ng/g), normal + T-2 toxin (100 ng/g), low Se, low Se + T-2 toxin (10 ng/g), and low Se + T-2 toxin (100 ng/g) groups. The pathological changes and fibrosis of spleen tissue were observed using hematoxylin-eosin (HE) staining and Masson staining, respectively. Mitogen-activated protein kinase p38 (p38 MAPK), phosphorylated protein-38 (P-p38 MAPK), nuclear factor kappa-B (NF-κB), and interleukin-6 (IL-6) expression levels in spleen tissues were analyzed by Western blotting (WB) and immunohistochemistry (IHC) staining. This study found that both Se deficiency and T-2 toxin induced inflammatory injury and fibrotic changes in rat spleen, but low selenium and low selenium combined with T-2 toxin intervention showed more intense splenic injury. Se deficiency combined with T-2 toxin intervention aggravated spleen injury, and the mechanism of occurrence involved an increase in the inflammatory injury in the spleen by elevating the expression levels of p38 MAPK, NF-κB, and IL-6 in rat spleen.