Rice prolamin extract ameliorates acute murine colitis by inhibiting nuclear factor‐kappa B and modulating intestinal apoptosis and cell proliferation

Summary We investigated the impact of rice prolamin extract ( RPE ) on lipopolysaccharide ( LPS )‐induced nuclear factor ( NF )‐κ B signalling in intestinal epithelial cells and macrophages, and determined the therapeutic efficacy of RPE in acute murine colitis. The effect of RPE on LPS ‐induced NF ‐κ B signalling and proinflammatory gene expression was evaluated by reverse transcription–polymerase chain reaction ( RT – PCR ), W estern blotting, immunofluorescence and electrophoretic mobility shift assay ( EMSA ). The in‐vivo efficacy of RPE was assessed in mice with 3% dextran sulphate sodium ( DSS )‐induced colitis. Apoptotic and cellular proliferative activities were evaluated by immunostaining with cleaved caspase‐3 and proliferating cell nuclear antigen ( PCNA ) antibodies. RPE inhibited LPS ‐induced expression of monocyte chemotactic protein ( MCP )‐1, interleukin ( IL )‐6 and tumour necrosis factor ( TNF )‐alpha and LPS ‐induced NF ‐κ B signalling in intestinal epithelial cells and macrophages. RPE ‐fed, DSS ‐exposed mice showed less weight loss, longer colon length and lower histological score compared to control diet‐fed, DSS ‐exposed mice. Immunostaining analysis revealed a significant decrease of cleaved caspase‐3 positive cells in RPE ‐fed, DSS ‐exposed mice compared to DSS ‐exposed mice. Also, the number of PCNA ‐positive cells within intact colonic crypts decreased significantly in RPE ‐fed, DSS ‐exposed mice compared to control diet‐fed, DSS ‐exposed mice. DSS ‐induced NF ‐κ B signalling was inhibited by RPE . RPE ameliorates intestinal inflammation by inhibiting NF ‐κ B activation and modulating intestinal apoptosis and cell proliferation in an acute murine colitis.