## 4 Discussion
Therefore, one of the targets of IBD prevention and treatment is to preserve the intestinal barrier function by upregulating tight junction proteins and inhibiting mTOR signaling [21]. Fucoxanthin and salicortin demonstrated the ability to inhibit the mTOR pathway [23; 60]; therefore, _S. horneri_ is a potential mTOR inhibitor that can be used to treat and/or prevent UC. In this study, SHE decreased mTOR and its downstream S6K in cell and animal experiments. In addition, ZO-1, a tight junction factor, was significantly elevated in cell experiments, whereas Claudin-1 and occludin were elevated in animal experiments. This is likely due to the fact that animals exhibited a greater variety of variables. The gut microbiota and immune system interact to maintain intestinal homeostasis; when this balance is disrupted, gut dysbiosis results in gut bacterial overgrowth, leading to intestinal barrier disruption and systemic translocation of pathogens [61]. Recent advances in IBD research have focused on modifying gut microbiota composition and gut dysbiosis, which is regulated by diet but not inheritance [62; 63]. According to previous studies, fucoida improved dysbiosis by decreasing harmful bacteria such as _Petococcus_ and increasing beneficial bacteria such as _Lactobacillus_ and _Ruminococcaceae_[64], and _S. horneri_ decreased the F/B ratio in high-fat-fed mice [32]. In our study, there was no difference in the Shannon index between the groups, and the DSS group showed an increased tendency in [PERSON]'s PD richness compared with that in the control group, whereas the \(\alpha\) diversity in the SHE treatment group was lower than that of the DSS group. The results of another study involving polyphenol-rich extracts and a DSS colitis model were comparable to our results. The Shannon index was unaffected by DSS treatment or the anti-inflammatory bioactive compound, but DSS increased [PERSON]'s PD richness, and the polyphenol-rich extract decreased it [65]. \(\beta\)-diversity analysis showed that SHE treatment regulated the gut microbiota composition differently than that of DSS treatment. At the phylum level, the F/B ratio is an indicator of normal intestinal homeostasis. An abnormal balance of the ratio indicates gut dysbiosis, and it has been reported that IBD patients have a lower F/B ratio than healthy individuals because _Faecalibacterium_ spp. are lowered and _Bacteroides_ spp. induced [66]. However, in our study, the F/B ratio increased with DSS treatment but decreased with SHE treatment. It was reported that the distribution of gut microbiota in DSS-induced colitis in mice differs from that of IBD patients [67]. The F/B ratio fluctuated weekly at 7, 14, 21 days after DSS administration, and especially the F/B ratio increased 7 days after DSS administration [67], consistent with our findings and those of other researches [68; 69]. _Bacteroides_ spp. and _Erysipelatoclostridium_ spp. are lactic acid bacteria and SCFA producers [70; 71]; their abundances decreased in the DSS-treated group but increased significantly in the SHE-treated group. In addition, the SHE-treated group had elevated levels of beneficial probiotics for maintaining intestinal homeostasis, including _Akkermansia muciniphala_, _Bifidobacterium bifidum_, and _Lactococcus lactis_[72; 73]. In conclusion,SHE treatment increased the abundance of beneficial bacteria. Although the benefits of SHE for improving intestinal health, reducing obesity, and acting as an antioxidant are well-established, this is the first study to examine how SHE affects UC while observing changes in the intestinal microbiome. One limitation of this experiment is that only male mice were used in this experiment because the prevalence of IBD is gender-specific. In the DSS-induced colitis model, female mice exhibited significantly fewer inflammatory symptoms than male mice (longer colon, lower body weight loss, lower TNF-\(\alpha\) level) and were partially protected against chemically induced colitis due to estradiol [74].