Search

In Lung adenocarcinoma (ADC), Qi-Yin deficiency syndrome (QY) is the most common Traditional Chinese medicine (TCM) syndrome. This study aimed to investigate the diversity and composition of gut microbiota in ADC patients with QY syndrome. 90 stool samples, including 30 healthy individuals (H), 30 ADC patients with QY syndrome, and 30 ADC patients with another syndrome (O) were collected. Then, 16s-RNA sequencing was used to analyze stool samples to clarify the structure of gut microbiota, and linear discriminant analysis (LDA) effect size (LEfSe) was applied to identify biomarkers for ADC with QY syndrome. Logistic regression analysis was performed to establish a diagnostic model for the diagnosis of QY syndrome in ADC patients, which was assessed with the AUC. Finally, 20 fecal samples (QY: 10; O: 10) were analyzed with Metagenomics to validate the diagnostic model. The α diversity and β diversity demonstrated that the structure of gut microbiota in the QY group was different from that of the H group and O group. In the QY group, the top 3 taxonomies at phylum level were Firmicutes, Bacteroidetes, and Proteobacteria, and at genus level were Faecalibacterium, Prevotella_9, and Bifidobacterium. LEfSe identified Prevotella_9 and Streptococcus might be the biomarkers for QY syndrome. A diagnostic model was constructed using those 2 genera with the AUC = 0.801, similar to the AUC based on Metagenomics (0.842). The structure of gut microbiota in ADC patients with QY syndrome was investigated, and a diagnostic model was developed for the diagnosis of QY syndrome in ADC patients, which provides a novel idea for the understanding and diagnosis of TCM syndrome. [ABSTRACT FROM AUTHOR]

Ulcerative colitis (UC) is a chronic and relapsing inflammatory bowel disorder in the colon and rectum leading to low life-quality and high societal costs. Ursolic acid (UA) is a natural product with pharmacological and biological activities. The studies are aimed at investigating the protective and treatment effects of UA against the dextran sulfate sodium- (DSS-) induced UC mouse model and its underlying mechanism. UA was orally administered at different time points before and after the DSS-induced model. Mice body weight, colon length, and histological analysis were used to evaluate colon tissue damage and therapeutic evaluation. Intestinal transcriptome and microbe 16 s sequencing was used to analyze the mechanisms of UA in the prevention and treatment of UC. The early prevention effect of UA could effectively delay mouse weight loss and colon length shorten. UA alleviated UC inflammation and lowered serum and colon IL-6 levels. Three classical inflammatory pathways: MAPKs, IL-6/STAT3, and PI3K were downregulated by UA treatment. The proportion of macrophages and neutrophils in inflammatory cell infiltration was reduced in UA treatment groups. UA could significantly reduce the richness of intestinal flora to avoid the inflammatory response due to the destruction of the intestinal epithelial barrier. The function of UA against UC was through reducing intestinal flora abundance and regulating inflammatory and fatty acid metabolism signaling pathways to affect immune cell infiltration and cytokine expression. [ABSTRACT FROM AUTHOR]