GABA‐enriched rice bran inhibits inflammation in LPS‐stimulated macrophages via suppression of TLR4‐MAPK/NF‐κB signaling cascades

Gamma‐aminobutyric acid (GABA)‐enriched products (GEP) exhibited a wide range of pharmaceutical properties. In this study, anti‐inflammatory activity of GEP from Lactobacillus fermentum‐fermented water solution of rice bran was evaluated on lipopolysaccharide‐activated macrophage model. GABA content in L. fermentum‐fermented rice bran solution was determined up to 1.27 g/L. GEP was shown to inhibit the expression levels of inducible nitric oxide synthase and cyclooxygenase‐2 enzymes. Moreover, pretreatment of GEP attenuated the generation level of interleukin (IL)‐6, IL‐1β, tumor necrosis factor α, and monocyte chemoattractant protein‐1. Especially, the activation of signaling pathways due to nuclear factor‐κB (NF‐κB) and mitogen‐activated protein kinases (MAPKs) was interrupted in GEP‐exposed cells. Notably, molecular docking result showed a potential binding of GABA to Toll‐like receptor 4 with a binding energy of −3.88 kcal/mol, suggesting the role of GABA in suppression of Toll‐like receptor 4‐MAPK/NF‐κB signaling cascades. As the result, GEP from L. fermentum‐fermented rice bran solution could be suggested as a promising food for suppression of inflammatory responses. Practical applications GABA‐enriched products have been evidenced to possess various pharmaceutical properties and health beneficial effects. In this study, GABA‐enriched product from L. fermentum‐fermented rice bran solution exhibited the inhibition on inflammatory response in macrophages. Hence, it could be used as a potential ingredient for the mitigation of inflammatory responses. In this study, anti‐inflammatory activity of GEP from Lactobacillus fermentum‐fermented water solution of rice bran was evaluated on lipopolysaccharide‐activated macrophage model. The anti‐inflammatory activity of GEP was determined due to suppressing Toll‐like receptor 4‐mitogen‐activated protein kinase/nuclear factor‐κB signaling cascades, leading to the attenuation of inflammatory mediator production.