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Background: Atractylodes lancea (AL) has been used in traditional Chinese medicine for the treatment of various diseases including digestive disorders. Ulcerative colitis (UC) is a common digestive system disease with a low cure rate and easy recurrence. However, it is still not clear whether AL is suitable for UC treatment. Currently, stir-baking with wheat bran is most commonly used to process AL. Here, we aimed to address the effects of the crude and bran-processed AL on UC in vitro and uncover the underlying mechanism based on regulating the IKK/NF-kappa B signaling pathway., Methods: Human colonic epithelial cells (HCoEpiC) were treated with lipopolysaccharide (LPS) to mimic the inflammatory injury of UC in vitro. The essential oil from crude and bran-processed AL was used to treat LPS-induced HcoEpiC cells. The cell viability was detected by an MTT assay. The levels of IL-4, IL-6, IL-8, IL-12, IL-1- β , TNF- α, and NO were determined by ELISA, and the mRNA expressions of IKK- α , NF- κ B, IL-4, IL-6, IL-8, and TNF- α were determined by RT-PCR. Meanwhile, the expressions of IKK- α , p-IKK- α , p-IKK- β , NF- κ B, IL-6, and IL-8 proteins were determined by Western blot., Results: The essential oil of AL, whether it was from crude or bran-processed AL, could significantly increase the viability of LPS-induced HCoEpiC cells. The treatment of AL essential oil also notably inhibited the productions of IL-6, IL-8, IL-12, IL-1- β , TNF- α , NO, p-IKK- α , p-IKK- β, and NF- κ B and downregulated the mRNA expressions of NF- κ B, IL-6, IL-8, and TNF- α . Meanwhile, IL-4 protein and mRNA expression were significantly stimulated by AL essential oil. Moreover, the essential oil from bran-processed AL was more effective than that from crude AL., Conclusion: Both kinds of AL essential oil had the anti-inflammatory effect on LPS-induced HCoEpiC, and the essential oil from bran-processed AL was more effective. The mechanism could be through the IKK/NF- κ B signaling pathway in vitro., Competing Interests: The authors declare that there are no conflicts of interest., (Copyright © 2021 Yan Yu et al.)

Diets high in animal fats are associated with increased risks of inflammatory bowel disease, but the mechanism remains unclear. In this study, we investigated the effect of high-fat diet (HFD) on the development of experimental colitis in mice. Relative to mice fed low-fat diet (LFD), HFD feeding for 4 wk increased the levels of triglyceride, cholesterol, and free fatty acids in the plasma as well as within the colonic mucosa. In an experimental colitis model induced by 2,4,6-trinitrobenzenesulfonic acid (TNBS), mice on 4-wk HFD exhibited more severe colonic inflammation and developed more severe colitis compared with the LFD counterparts. HFD feeding resulted in higher production of mucosal pro-inflammatory cytokines, greater activation of the myosin light chain kinase (MLCK) tight junction regulatory pathway, and greater increases in mucosal barrier permeability in mice following TNBS induction. HFD feeding also induced gp91, an NADPH oxidase subunit, and promoted reactive oxygen species (ROS) production in both colonic epithelial cells and lamina propria cells. In HCT116 cell culture, palmitic acid or palmitic acid and TNF-α combination markedly increased ROS production and induced the MLCK pathway, and these effects were markedly diminished in the presence of a ROS scavenger. Taken together, these data suggest that HFD promotes colitis by aggravating mucosal oxidative stress, which rapidly drives mucosal inflammation and increases intestinal mucosal barrier permeability. NEW & NOTEWORTHY This study demonstrates high-fat diet feeding promotes colitis in a 2,4,6-trinitrobenzenesulfonic acid-induced experimental colitis model in mice. The underlying mechanism is that high-fat diet induces oxidative stress in the colonic mucosa, which increases colonic epithelial barrier permeability and drives colonic mucosal inflammation. These observations provide molecular evidence that diets high in saturated fats are detrimental to patients with inflammatory bowel diseases.