Walnut oil alleviates LPS-induced intestinal epithelial cells injury by inhibiting TLR4/MyD88/NF-κB pathway activation

In this study, we investigated the protective effects of walnut oil (WO) on mouse intestinal epithelial cells using used MODE-K cells as a model and explored the underlying mechanisms. Our data suggested that WO attenuated lipopolysaccharide (LPS)-induced pathological changes and inhibited the rate of LPS-induced apoptosis in MODE-K cells. Furthermore, WO down-regulated LPS-induced gene and protein expression of toll-like receptor 4 (TLR4), myeloid differentiation primary response gene 88 (MyD88), nuclear factor-kappa B (NF-kappa B), tumor necrosis factor-alpha, and interleukin-6. In conclusion, this study shows that WO exerts an anti-inflammatory effect on LPS-induced MODE-K cells injury by inhibiting the TLR4/MyD88/NF-kappa B pathway activation. Based on our data, a prominent functional food candidate can be provided for inflammatory bowel disease treatment. Practical applications Walnut oil (WO) has excellent anti-inflammatory properties and is widely used in traditional dietary supplements. However, whether WO causes anti-lipopolysaccharide (LPS)-induced intestinal injury remains unclear. In this study, we investigated the protective effects of WO on mouse intestinal epithelial cells using MODE-K cells as a model and explored their potential mechanisms. Our data showed that WO ameliorated the pathological morphology, inhibited the apoptosis of LPS-induced MODE-K cell injury, decreased the release of pro-inflammatory cytokines, and down-regulated the related genes and proteins expression of the LPS-TLR4/MyD88/NF-kappa B inflammatory pathway. The results of this study would enhance the utilization of WO in the prevention of gastrointestinal diseases in animals and humans inflammatory bowel disease as well as in functional foods formulations.