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Crohn's disease (CD) is a chronic relapsing form of inflammatory bowel disease, and its pathogenesis remains unknown. Total flavone of Abelmoschus manihot L. Medic (TFA), has been used as anti‑inflammatory and myocardial ischemia protective drug. The present study aimed to explore the effects of TFA on CD and its underlying mechanism. We reported that TFA comprises eight flavone glycosides, including quercetin‑3‑O‑robinobioside, gossypetin‑3‑O‑glucoside, quercetin‑3'‑O‑glucoside, isoquercetin, hyperoside, myricetin, gossypetin and quercetin. In vivo, TFA promoted the survival of 2,4,6‑trinitrobenzene sulfonic acid (TNBS)‑induced colitis in mice, decreased weight loss and increased colon length in a dose‑dependent manner. Additionally, TFA notably ameliorated the inflammatory response in mice with TNBS‑induced colitis as determined by histopathological analysis. In addition, the administration of TFA in mice with TNBS‑induced colitis led to a significant decrease in the levels of cytokines in the sera and colon tissues; a significant decrease myeloperoxidase activity in the colon tissues was also observed. These findings may be associated with the suppression of the nuclear factor‑κB (NF‑κB) and mitogen‑activated protein kinase (MAPK) signaling pathways. In vitro, TFA significantly downregulated the expression of cytokines in lipopolysaccharide (LPS)‑induced RAW264.7 cells. In addition, TFA suppressed LPS‑induced activation of the NF‑κB and MAPK signaling pathways in RAW264.7 cells. Our findings indicated that TFA could suppress the inflammatory response in mice with TNBS‑induced colitis via inhibition of the NF‑κB and MAPK signaling pathways. The results of the present study may improve understanding of the function of TFA and provide a novel theoretical basis for the treatment of CD.

Total flavone of Abelmoschus manihot ameliorates Crohn's disease by regulating the NF‑κB and MAPK signaling pathways