TJP1 (Tight Junction Protein 1)

BXD intervention demonstrated significant therapeutic effects in GPL mice. The underlying mechanisms are associated with the restoration of gastric microbiota dysbiosis, promotion of beneficial bacterial growth, suppression of potential pathogens, modulation of the inflammatory response, and alleviation of mucosal damage.

Concurrently, maternal CUR increased the relative abundance of Lactobacillus (P < 0.05), which was negatively correlated with intestinal inflammation and oxidative stress. The present study showed that maternal CUR supplementation can alleviate intestinal inflammation in offspring chickens, which may be mediated by regulating gut microbiota composition.

Additionally, organ-on-a-chip technology confirmed that SFALCA showed no significant toxicity to the liver. In conclusion, this study elucidates the active components and mechanisms of SFALCA in treating IBD and assesses its safety, providing a reliable in vitro platform for future therapeutic strategies.

In pregnant mice, maternal DHA supplementation mitigated LPS-induced FGR by suppressing NF-κB-mediated inflammatory signaling, modulating gut microbiota composition, and supporting intestinal barrier function, highlighting a potential nutritional strategy to alleviate inflammation-associated adverse pregnancy outcomes.

PPE mitigates inflammation and oxidative stress, restoring intestinal barrier function. The beneficial effects induced by the extract could be related to the pattern of polyphenolic composition, with particular regard to HT, rosmarinic acid, p-coumaric acid, catechin, as well as punicalagins A and B.

SPIOCA gavage fortified intestinal barrier integrity-evidenced by elevated ZO-1, ZO-2, Occludin and Claudin-1 expression-and potentiated antitumor immune-cell infiltration, specifically by CD8+ T cells and dendritic cells, into the tumor microenvironment. We therefore preliminarily conclude that SPIOCAs restore gut microbiota homeostasis in lung cancer, thereby enhancing intestinal barrier integrity and converting the tumor immune microenvironment from an immune desert to an immune-inflamed phenotype, ultimately improving lung cancer immunotherapy efficacy.

Furthermore, they acted together on the p38 mitogen-activated protein kinase (MAPK) signaling pathway, and the addition of the p38 inhibitor SB203580 partially inhibited the expression of p38MAPK. Thus, the combined action of these drugs protected the NVU.

Our findings suggest that DMBX1 may have potential as a prognostic biomarker for prognostic assessment in colon cancer and is associated with alterations in the tumor immune microenvironment.Mechanistically, DMBX1 likely primarily influences the occurrence and development of colon cancer by promoting the invasion and migration of colon cancer cells.

On the other hand, in vivo experiments revealed that brexpiprazole significantly inhibited the formation of CRC lung metastases, suppressed the expression of SREBP1(m), SNAI1and MMP9, and upregulated the expression of E-Cad and ZO1. Brexpiprazole inhibits the migration, invasion and metastasis of CRC cells by inhibiting the SREBP1/SNAI1 signalling pathway and downregulating the expression of EMT-related factors.

Our findings disclose that GAA alleviated DSS-induced UC by inhibiting the IL-17 signaling pathway via targeting RORA to reduce inflammation. Our study suggests that GAA holds potential as a nutritional intervention for the prevention and treatment of UC.

Baizhi alleviates migraine through multi-target regulation of the gut-brain axis, including intestinal barrier repair, gut microbiota remodeling, and cerebral metabolic restoration. Notably, this study on Baizhi represents the first integration of spatial metabolomics (MALDI-MSI) with gut microbiome and systemic metabolomics to elucidate migraine mechanisms, providing a novel multi-omics strategy for understanding the holistic therapeutic effects of traditional Chinese medicine. These findings provide a mechanistic basis for its clinical application in migraine treatment.

This proteogenomic framework defines exposure-informed and microbiome-informed gastric cancer subtypes, providing a molecular schema for patient stratification, prevention and actionable therapeutic vulnerabilities.