We investigated how inulin-type fructan CP-A, a key component found in certain polysaccharides, influences ulcerative colitis (UC), an inflammatory disease marked by symptoms like abdominal pain, diarrhea, and bloody stools. To conduct this research, we used a rat model treated with 2,4,6-trinitrobenzene sulfonic acid (TNBS) to simulate UC and an in vitro model with colonic epithelial cells exposed to lipopolysaccharides (LPS) to better understand the cellular response.
Through our experiments, we discovered that CP-A significantly lessens colonic injuries and reduces markers associated with inflammation, such as interleukin-8 and tumor necrosis factor-alpha. Furthermore, we observed improvements in levels of protective substances like interleukin-10 and transforming growth factor-beta after treatment with CP-A. In our in vitro tests, CP-A effectively lowered nitric oxide and interleukin-1 beta production following LPS stimulation, indicating a reduction in inflammatory responses.
Our metabolic analysis revealed a connection between CP-A therapy and the mammalian target of rapamycin (mTOR) signaling pathway. Both in vivo and in vitro validations suggested that this pathway plays a critical role in CP-A's ability to alleviate UC by inhibiting inflammation-related signaling mechanisms. These findings can pave the way for new treatment approaches for patients suffering from ulcerative colitis, suggesting that inulin-type fructan CP-A holds therapeutic promise in managing and potentially improving this challenging condition.
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