The widespread occurrence of nanoplastics (NPs), has markedly affected the ecosystem and has become a global threat to animals and human health. There is growing evidence showing that
polystyrene nanoparticles (PSNPs) exposure induced
enteritis and the intestinal barrier disorder.
Lipopolysaccharide (LPS) can trigger the
inflammation burden of various tissues. Whether PSNPs deteriorate LPS-induced intestinal damage via ROS drived-NF-κB/NLRP3 pathway is remains unknown. In this study, PSNPs exposure/PSNPs and LPS co-exposure mice model were duplicated by
intraperitoneal injection. The results showed that exposure to PSNPs/LPS caused duodenal
inflammation and increased permeability. We evaluated the change of duodenum structure, oxidative stress parameters, inflammatory factors, and
tight junction protein in the duodenum. We found that PSNPs/LPS could aggravate the production of ROS and oxidative stress in cells, activate NF-κB/NLRP3 pathway, decrease the expression
tight junction proteins (ZO-1,
Claudin 1, and
Occludin) levels, promote inflammatory factors (TNF-α, IL-6, and IFN-γ) expressions. Duodenal oxidative stress and
inflammation in PS + LPS group were more serious than those in single exposure group, which could be alleviated by
NF-kB inhibitor QNZ. Collectively, the results verified that PSNPs deteriorated LPS-induced
inflammation and increasing permeability in mice duodenum via ROS drived-NF-κB/NLRP3 pathway. The current study indicated the relationship and molecular mechanism between PSNPs and intestinal injury, providing novel insights into the adverse effects of PSNPs exposure on mammals and humans.