This study investigated the effect of scallop plasmalogen (SP) on intestinal barrier function and the potential role of the gut microbiota in this effect. C57BL/6J male mice were divided into four groups, which were fed respectively with a low-fat diet (LFD), a high-fat diet (HFD), LFD + SP, and LFD + SP. Immunohistochemical staining and 16S rRNA sequencing were used to evaluate the effect of SP on growth index, serum inflammatory factor levels, intestinal permeability, intestinal barrier function and gut microbiota. The results showed that SP reduced the liver index and lowered serum proinflammatory factor levels in HFD-fed mice. SP also improved intestinal permeability, as evident by a decrease in the serum level of lipolyaccharide and a reduction in the circulating level of fluorescein isothiocyanate (FITC)-dextran in HFDfed mice. Meanwhile, SP maintained the structural morphology of the ileum and increased the ratio of villus height to crypt depth in HFD-fed mice. This may be attributed to the protective effect of SP on intestinal barrier function. SP alleviated intestinal mucosal barrier damage, restored the number of ileal goblet cells, protected the integrity of the intestinal epithelial barrier, and reversed the decrease in zonula occludens-1 (ZO-1) and occludin expression. Furthermore, SP significantly regulated the intestinal microbial composition, promoting the proliferation of beneficial bacteria related to intestinal barrier function, such as Colidextribacter and Lachnospiraceae_NK4A136_group. In summary, SP has protective effect against intestinal barrier damage and gut microbiota dysbiosis, and thus maintains intestinal health.

Both microbes and the hydrophobic antioxidant astaxanthin (AST) are promising tools for the treatment of inflammatory bowel disease (IBD) and colorectal cancer (CRC), but clinical use is still limited. Synergistic application and co-delivery of the two are valuable for broadening both microbial and antioxidant therapies. It is necessary to find a solution for co-delivery that kills two birds with one stone for effective intestinal delivery. In this study, a simple to prepare and stable liposomal system (Lipo@AST@PRO) has constructed for co-delivery of a microbial consortium and astaxanthin. For microbes: it provided microbial gastrointestinal protection and prolonged microbial intestinal retention. For astaxanthin: it exhibited good colonic release and bad odors masking effect.

Lipo@AST@PRO demonstrated dextran sulfate sodium (DSS)-induced colitis relief by restoring the intestinal barrier and the recovery of intestinal stem cells (ISCs). It also demonstrated synergistic antitumor efficacy with 5-fluorouracil (5-FU) in CT26 tumor-bearing mice by modulating the immune microenvironment and promoting vascular normalization. In conclusion, a platform was established for the co-delivery of multiple microorganisms and xenobiotics, which was beneficial for the intestinal illness. It broadened the therapeutic forms of intestinal diseases and provided a new reference for the application of microbial and hydrophobic antioxidants in food and drug forms.

It is unclear how docosahexaenoic acid (DHA) improves insulin resistance via modulating gut microbiome in obese individuals. We used diet-induced obesity (DIO) mice as a model to study the effects of DHA-rich fish oil (DHA-FO) on host metabolic disorders and colonic microbiome. DHA-FO reduced fat deposition, regulated lipid profiles and alleviated insulin resistance in DIO mice. Probably because DHA-FO prevented the permeation of lipopolysaccharide across intestinal epithelial barrier, and promoted peptide YY (PYY) secretion via the mediation of short chain fatty acids receptor (FFAR2) in colon. Furthermore, DHA-FO might regulate PYY expression by reversing microbial dysbiosis, including increasing the abundance of Akkermansia muciniphila and Lactobacillus, and suppressing the growth of Helicobacter. DHA-FO also altered gut microbial function (e.g. "linoleic acid metabolism") associated with PYY expression (r > 0.80, P < 0.05). Herein, DHA-FO enhanced insulin action on glucose metabolism by altering gut microbiome and facilitating colonic PYY expression in DIO mice.