The roles of exosomes in esophageal cancer.

The incidence and mortality rate of esophageal cancer (EC) are higher worldwide. Exosomes are nanoscale vesicles derived from various types of cells, exhibiting a stable presence in bodily fluids, and contain a plethora of bioactive components including proteins, DNA, and RNA. Exosomes can mediate cell-to-cell communication and signaling. Numerous studies conducted both domestically and internationally have indicated the significant involvement of exosomes in tumor development and their potential as novel diagnostic and prognostic biomarkers for liquid biopsy. This review seeks to consolidate the role of exosomes and bioactive substances in the progression of EC and elaborate on the opportunities and challenges associated with the clinical application of exosomes in EC.

Fructus ligustri lucidi suppresses inflammation and restores the microbiome profile in murine colitis models.

BACKGROUND: Ulcerative colitis (UC) is pathologically characterized by an inappropriate immune response to the gut commensal microbes accompanied by persistent epithelial barrier dysfunction, and its progression increases the susceptibility to colitis-associated cancer (CAC), as well as other complications. Fructus ligustri lucidi (FLL) has a long historical application in traditional Chinese medicine due to its various pharmacological effects, including antioxidation and anti-inflammation. The present study aimed to explore the molecular and cellular mechanisms of FLL in treating colitis. METHODS: A high-performance liquid chromatography (HPLC) combined with ultraviolet (UV) was performed to validate the quality of FLL; Network pharmacology analysis and weighted gene co-expression network analysis (WGCNA) based on The Cancer Genome Atlas (TCGA) database predicted the therapeutic value of FLL against UC and CAC; 2% dextran sodium sulfate (DSS) was administered to mice to establish murine models of experimental colitis, and FLL was given for the next 14 days at different concentrations; 16S rRNA sequencing and untargeted metabolomics were performed on fecal samples to delineate the alteration in microbiome profile; Western blotting, flow cytometry, and immunocytochemistry experiments were conducted to confirm the predicted cellular mechanisms. RESULTS: Network pharmacology analysis and WGCNA predicted that the targets of the FLL were associated with the progression of UC and the survival of patients with colorectal cancer by regulating tumor necrosis factor (TNF) and IL-17 signaling pathways, immune cell functions, responses to bacterial and reactive oxygen species (ROS), and cell proliferation. In vivo experiments corroborated that the high dose of FLL significantly attenuated the progression of experimental colitis by reversing the weight loss and bloody stool, reconstructing the integrity of colorectal epithelium, and suppressing the concentration of pro-inflammatory cytokines. Moreover, FLL treatment reduced the transition of macrophages (Mφs) to the proinflammatory phenotype and promoted Mφs-regulated wound healing, and suppressed the production of ROS in intestinal organoids (IOs) and crypts. 16S rRNA and untargeted metabolomics showed that the administration of FLL inhibited DSS-caused colonization of the potentially pathogenic gut microorganisms and reversed DSS-influenced metabolic profile. CONCLUSION: FLL is a potent anti-colitis drug by suppressing inflammation and rescuing dysbiosis.

Molecular epidemiology of astrovirus infection in infants in Wuhan, China.

We report the molecular epidemiology of astrovirus infection in 335 infants with diarrhea in Wuhan City, China. Astrovirus RNA was detected in the stool specimens of 33 children (9.87%). Genotyping analysis indicated that 23 out of 24 astroviruses identified were classified as belonging to genotype 1, with highest identity (>98%) to a Mongolian strain.