Acai berry extract as a regulator of intestinal inflammation pathways in a Caco-2 and RAW 264.7 co-culture model.

Abstract

The aim of this study was to assess the anti-inflammatory effects of acai berries in a Caco-2 and RAW 264.7 macrophage co-culture model. The acai berry extract (ABE) was prepared using 70% ethanol, and total anthocyanin, polyphenol, and flavonoid contents in ABE were analyzed. To the antioxidant activity of ABE, we measured radical scavenging activity as well as ferric reducing antioxidant power values. Prior to inducing inflammation, Caco-2 cells were co-cultured with RAW 264.7. Inflammation was induced using lipopolysaccharides (LPS) in RAW 264.7 cells. The transepithelial electrical resistance value was significantly recovered and the mRNA level of tight junction proteins, including ZO-1, JAM-1, and claudin-4, tended to increase compared with that in the LPS group. LPS-induced interleukin (IL)-6, IL-8, and prostaglandin E2 levels reduced significantly following treatment with the highest ABE concentration. In the highest ABE concentration, the phosphorylation of p65, p38 mitogen-activated protein kinase, and c-Jun N-terminal kinase was downregulated compared with the LPS group. The phosphorylation of extracellular signal-regulated kinase showed a decreased tendency. These results suggest that acai berry may improve gastrointestinal health. PRACTICAL APPLICATIONS: Acai berry is known to have abundant anthocyanin, which has many biological activities, including anti-inflammatory, antioxidant, antihypertensive, and anticytotoxic/cytoprotective activities. This study demonstrated the anti-inflammatory effects of acai berry extracts via TEER value, expression of tight junction protein, and production of inflammatory mediators and cytokines in the Caco-2 and RAW 264.7 co-culture model. Therefore, acai berry has the potential to prevent intestinal inflammatory diseases.