L.acidophilus combined with HKL alleviated colon inflammation in rats by inhibiting JAK2-STATI and affecting taurine metabolism

Objective To explore the therapeutic mechanism of L.acidophilus combined with Traditional Chinese Medicine Huan Kui Le(HKL) on ulcerative colitis(UC) by intestinal flora,intestinal immunity and metabolism. Methods The male Wistar rats were selected and randomly divided into Control group, UC Group, HKL Group, Lac Group, Lac + HKL Group (LH Group), and 5-ASA group. The UC model was established by TNBS/ethanol method in all groups except the Control group. After the model was successfully established, the corresponding drugs were administered intragastrically for 14 days. The expression of JAK2, STAT1, and STAT3 was detected by immunohistochemistry(IHC). The metagenomic technique was used to analyze fecal microbiome formation and function changes in UC rats after LH Tretment. Result The IHC results showed that the expression of JAK2 and STAT1 protein was down-regulated after LH intervention, but the expression of STAT3 protein was not significantly changed.The abundance of genes related to taurine metabolism was significantly higher in the UC group, while the abundance of related genes decreased after LH intervention. GT45, GH114, GH104, and PL3 were highly expressed in the UC group, while the expression was downregulated after LH intervention. Staphylococcus is a major contributor to the expression of carbohydrate related genes. Conclusion The LH Treatment can affect the composition of intestinal flora in UC rats and inhibit JAK2-STAT1 signal pathway.LH treatment can inhibit the abnormal increase of taurine metabolism in the gut of UC rats. • This paper focuses on the effect of the combination of Chinese medicine And probiotics on ulcerative colitis, We advanced that taurine metabolism and JAK-STAT signaling pathway may be key targets for treatment of ulcerative colitis. • Combined therapy: Investigates the synergistic effect of Chinese medicine and probiotics on ulcerative colitis (UC). • Key mechanism: Proposes taurine metabolism and JAK-STAT signaling pathway as potential therapeutic targets for UC. • Novelty: Provides new insights into the integrative treatment of UC using natural compounds and microbiota modulation.