To investigate the protective effect of β-glucan (BG) against intestinal ischemia reperfusion (Ⅱ/R) injury by regulating the secretion of glucagon-like peptide-1 (GLP-1).

Male C57BL/6 mice (6~8 weeks old) were subjected, and finally, the experiments had sham group, Ⅱ/R group, Ⅱ/R+BG group (0.1 mg/mL BG in drinking water for 2 weeks before modeling), Ⅱ/R+liraglutide (LLT, GLP-1 analogue) group (0.2 μg/g LLT injected every 12 hours for 3 consecutive days before modeling), and Ⅱ/R+BG+Ex9-39 (GLP-1R antagonist) group (intraperitoneal injection of 2 μg/g Ex9-39 1 h before modeling). After modeling, HE staining was used to observe intestinal morphological changes, and RT-qPCR and Western blotting were employed to evaluate the molecules (Occludin, ZO-1 and Claudin-1) related to intestinal barrier damage. The effect of 0.1 mg/mL BG treatment on the GLP-1 level in the serum and intestinal tissues of normal mice was determined with ELISA and immunofluorescence assay, respectively, and RT-PCR for the molecules related to GLP-1 expression (Gcg, Pcsk1/2, GIP and Foxa2). The effects of LLT and Ex9-39 pretreatment on intestinal morphology and intestinal barrier damage were also determined by morphological observation and expression levels of related molecules.

Ⅱ/R induced significant decreases in the mRNA levels of Occludin, ZO-1 and Claudin-1 and increase in Chiu’s score when compared with sham control mice (P<0.05). While, the mRNA levels of the 3 molecules were obviously higher and the Chiu’s score was lower in the Ⅱ/R+BG group than the Ⅱ/R group (P<0.05). BG pretreatment induced notably enhanced secretion of GLP-1 in the serum and intestinal tract of normal mice, and improved the mRNA expression of GLP-1-related molecules (P<0.05). The intervention of GLP-1 analogue LLT could attenuate the Ⅱ/R damage and decreased Chiu’s score, with statistical difference in comparison with the Ⅱ/R group (P<0.05). GLP-1 receptor antagonist Ex9-39 reversed the protective effects of BG pretreatment against Ⅱ/R damage, with notably differences in the expression of Occludin, ZO-1 and Claudin-1 and Chiu’s score (P<0.05).

BG can attenuate intestinal mucosal and functional injury after Ⅱ/R by promoting intestinal GLP-1 secretion.

To analyze the diversity and composition changes of gut fungal communities between mouse model of total parental nutrition (TPN) and normal control mice.

After mouse model of TPN was constructed, fresh feces were collected from TPN mice (n=5) and normal control mice (n=5). Internal transcribed spacer (ITS) DNA sequencing was applied to determine intestinal fungi, and then bioinformatics analysis was conducted to identify the differences in fungal diversity, structure, and functional properties between the 2 groups of mice.

There were significant differences in Alpha diversity (P<0.05) and Beta diversity (P<0.01) of intestinal fungi between the 2 groups. In the TPN model group, the relative abundances of Candida, Penicillium, Aspergillus and Talaromyces were obviously reduced (all P<0.01). LEfSe analysis indicated that the above 4 strains were notably enriched in the normal control mice.

TPN mice exhibit characteristic changes in the composition of gut fungal flora compared to normal control mice. Dysfunction of gut fungal community may promote the occurrence of TPN related complications, and regulating the balance of gut fungal community may become a new strategy for preventing TPN related complications.

To investigate the role and physiological significance of transient receptor potential vanilloid receptor 4（TRPV4）in regulation of calcium influx in rat intestinal glial cells.

The expression of TRPV4 at mRNA and protein levels and its localization were detected by RT-qPCR, Western blotting and immunofluorescence assay in rat enteric glial cell line CRL-2690, rat intestinal epithelial cell line IEC6 and human embryonic kidney cell line HEK293T. The CRL-2690 cells were divided into GSK1016790A（GSK, TRPV4-specific agonist）group and GSK+HC067047（HC, TRPV4-specific inhibitor）group, hypotonic group and hypotonic+HC group, GdCl₃ group and GdCl₃+HC group, and CaCl₂ group and CaCl₂+HC group, while the activity of TRPV4 channel was assessed by Fura-2 fluorescent probe and single-cell fluorescent calcium ion assay. CRL-2690 cells were also divided into control group, GSK group and GSK+HC group, and the level of cellular ATP release was measured by luciferin-luciferase assay, and the mRNA levels of inflammatory genes GFAP, IL-1β, IL-6 and IL-10 were detected by RT-qPCR.

TRPV4 was expressed at mRNA and protein levels in rat intestinal glial cell line CRL-2690. GSK and low osmolarity stimulation significantly enhanced intracellular calcium fluorescence intensity in CRL-2690 cells, which was inhibited by HC（0.430 38±0.063 65 vs 0.004 23±0.005 78, P<0.000 1）. Calcium-sensing receptor（CaSR）activation-induced Ca²⁺ influx was also inhibited by HC（P<0.05）. Functionally, activation of TRPV4 promoted ATP release, expression of EGC reactive proliferation marker, GFAP, and inflammatory factors IL-1 β as well as IL-6, and inhibited the expression of anti-inflammatory factor IL-10 respectively. But all these effects were inhibited by HC treatment（P<0.05）.

Activation of TRPV4 induces extracellular Ca²⁺ influx and promotes ATP release and expression of inflammatory cytokines in enteric glial cell, which may be closely involved in the underlying mechanisms of bowel inflammation.