Surface-Layer Protein from <i>Lactobacillus acidophilus</i> NCFM Inhibits Lipopolysaccharide-Induced Inflammation through MAPK and NF-κB Signaling Pathways in RAW264.7 Cells

Abstract

The objective of our research was to evaluate the molecular mechanism of the anti-inflammatory effects of surface-layer protein (Slp) derived from Lactobacillus acidophilus NCFM in lipopolysaccharide-induced RAW264.7 cells. Our results presented that Slp, with an apparent size of 46 kDa, attenuated the production of TNF-α, IL-1β, and reactive oxygen species (ROS), by inhibiting the MAPK and NF-κB signaling pathways. In addition, 10 μg mL^-1 of Slp significantly inhibited NO and PGE₂ production ( P < 0.001) through downregulating the expression levels of iNOS and COX-2 protein. Furthermore, Slp was found to inhibit NF-κB p65 translocation into the nucleus to activate inflammatory gene transcription. These findings suggest that Slp is a potential immune-modulating bioactive protein derived from probiotics and holds promise for use as an additive in functional foods.