Porous Se@SiO2 nanospheres attenuate cerulein-induced acute pancreatitis in mice via downregulation of oxidative stress.

Objective Acute pancreatitis (AP) is a common digestive tract disease caused by gall stone obstruction, alcoholism and other factors. Pancreatitis may develop into severe pancreatitis, which has a relatively high mortality rate. Thus, effective methods for treating it need to be developed. Our study tried to assess the protective effect of Se@SiO2 nanospheres on AP. Methods Cerulein injection was used to induce acute pancreatitis. C57bl/6 mice were pretreated with Se@SiO2 nanocomposites at 1 and 2 mg/kg. Plasma amylase and lipase, inflammatory cytokines, alanine aminotransferase (ALT), aspartate aminotransferase (AST), blood urea nitrogen (BUN), and Sr were evaluated for each group. Immunofluorescence assay of reactive oxygen species (ROS), myeloperoxidase (MPO), and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling was conducted, and levels of MPO, MDA, SOD, GSH were evaluated. Finally, Western blot analysis was used to evaluate the effects of Se@SiO2 nanoparticle on the protein levels of Nrf2, HO-1, and NQO1 protein as well as TLR4, Myd88, and P-P65 protein in pancreatic tissues. Results Se@SiO2 nanocomposites alleviated the pathological damage to the pancreas as well as lungs during pancreatitis. Se@SiO2 nanocomposites evidently affected the reduction of pancreatic enzymes and inflammatory cytokines (IL-6, IL-1β, TNF-α). Se@SiO2 nanocomposites also can reduce other organs injury such as the liver and kidneys (as indicated by lower ALT, AST, BUN, and Sr levels). Moreover, Se@SiO2 nanocomposites reduced oxidative stress. Se@SiO2 nanocomposites ultimately inhibited TLR4/ Myd88/p-p65 pathway and increased the level of NQO1, Nrf2, and HO-1 protein. Conclusion In conclusion, Se@SiO2 nanocomposites exerted a protective effect on acute pancreatitis.