AI Article Synopsis
- The study examined the effectiveness of two compounds, FL-276.1 and FL-228.1, in reducing colitis induced by dextran sulfate sodium (DSS).
- Both compounds showed significant improvement in colitis symptoms, whether administered throughout the experiment or after DSS treatment began.
- The compounds activated certain cellular pathways (AHR and NRF2), helped regulate inflammation, and improved gut barrier function by increasing tight junction proteins, supporting future probiotic development for colitis treatment.
Article Abstract
In this study, the effectors and mechanisms of FL-276.1 and FL-228.1 in alleviating dextran sulfate sodium (DSS)-induced colitis were investigated. Both FL-276.1 and FL-228.1 significantly alleviated DSS-induced colitis, whether they were supplemented from the beginning of the experiment (whole course intervention) or after the DSS induction started (partial intervention). Aryl hydrocarbon receptor (AHR) and the nuclear factor erythroid 2-related factor 2 (NRF2) pathways were activated in mice colons, while the NLR family pyrin domain containing 3 (NLRP3) was downregulated under the whole course intervention modes. Indole-3-lactic acid, an AHR ligand produced by FL-276.1 and FL-228.1, could regulate the AHR/NRF2/NLRP3 pathway in Caco-2 monolayers, thus upregulating the tight junction proteins and protecting the integrity of the epithelial barrier. These results are conducive to promoting clinical trials and product development of probiotics for alleviating colitis.
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| http://dx.doi.org/10.1021/acs.jafc.2c06894 | DOI Listing |
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