Vortioxetine hydrobromide is a common clinical medication for major depressive disorder (MDD). However, it remains unclear whether vortioxetine hydrobromide acts by affecting the structure and composition of gut microbiota. Here, we analyzed fecal samples from 28 healthy controls (HCs) and 26 patients with MDD before treatment with vortioxetine hydrobromide, at 4 weeks after treatment, and at 8 weeks after treatment. High-throughput pyrosequencing showed that, according to the Chao1 and Shannon indices, fecal bacterial α-diversity was higher in the patients with MDD than in the HCs (p < 0.05), but no significant differences were observed after vortioxetine hydrobromide treatment (p > 0.05). PCoA results revealed that the gut microbiota composition was significantly different between the MDD groups and HCs. Proteobacteria and Actinobacteria were strongly increased, whereas Firmicutes were significantly reduced in the MDD group compared with the HCs. After treatment with vortioxetine hydrobromide, Firmicutes were significantly increased, and the proportion of Bacteroidetes decreased. Most notably, Lachnospira, Roseburia, and Faecalibacterium were negatively correlated with the severity of depressive symptoms. Taken together, our data indicate changes in the fecal microbiota composition in MDD patients compared with HCs, and vortioxetine hydrobromide may treat MDD through regulation of the gut microflora.

Background. The diagnosis of NAFLD requires a liver biopsy, which is difficult in children. This study explored the diagnostic value of pentraxin 3 (PTX-3) and the triglyceride-glucose (TyG) index for NAFLD in children. Methods. Sixty-eight children with NAFLD were selected as study subjects, and 68 healthy children enrolled during the same period served as controls. The TyG index was calculated, serum PTX-3 expression was detected by enzyme-linked immunosorbent assay, and the correlations between PTX-3 or the TyG index and clinical and biochemical indicators were analyzed. A receiver operating characteristics curve analysis and area under the curve (AUC) were used to evaluate diagnostic accuracy. Results. Serum PTX-3 level and the TyG index of the NAFLD patients were significantly higher than those of the healthy controls ( ), which was closely related with the BMI, ALT, and insulin resistance. The AUC of PTX-3 for diagnosing NAFLD was 0.731 (95% confidence interval [CI] 0.646-0.806), and the AUC of the TyG index for diagnosing NAFLD was 0.765 (95% CI 0.682-0.835). The AUC of PTX-3, the TyG index, and ALT for the combined diagnosis of NAFLD was 0.964 (95% CI 0.916-0.989). Conclusion. PTX-3 and the TyG index are novel diagnostic biomarkers for NAFLD, as they effectively improved the diagnostic accuracy for NAFLD when combined with ALT.

Background: There is no direct evidence of gut microbiota disturbance in children with gastroesophageal reflux disease (GERD). This study aimed to provide direct evidence and a comprehensive understanding of gut microbiota disturbance in children with GERD through combined metagenomic and metabolomic analysis.Methods: 30 children with GERD and 30 healthy controls (HCs) were continuously enrolled, and the demographic and clinical characteristics of the subjects were collected. First, 16S rRNA sequencing was used to evaluate differences in the gut microbiota between children with GERD and HC group, and 10 children with GERD and 10 children in the HC group were selected for metagenomic analysis. Nontargeted metabolomic analysis was performed using liquid chromatography/mass spectrometry (LC/MS), and metagenomic and metabolomic data were analyzed together.Results: There were significant differences in the gut microbiota diversity and composition between children with GERD and HCs. The dominant bacteria in children with GERD were Proteobacteria and Bacteroidota. At the species level, the top three core bacterial groups were Bacteroides stercoris, Bacteroides vulgatus and Alistipes putredinis. The main differential pathways were identified to be related to energy, amino acid, vitamin, carbohydrate and lipid metabolism. LC/MS detected 288 different metabolites in the positive and negative ion modes between children with GERD and HCs, which were mainly involved in arachidonic acid (AA), tyrosine, glutathione and caffeine metabolism.Conclusion: This study provides new evidence of the pathogenesis of GERD. There are significant differences in the gut microbiota, metabolites and metabolic pathways between HCs and children with GERD, and the differences in metabolites are related to specific changes in bacterial abundance. In the future, GERD may be treated by targeting specific bacteria related to AA metabolism.

Aim. Chlorogenic acid (CGA) is a natural polyphenolic compound found in human dietary products. Previous studies have confirmed that CGA has many biological activities, such as regulating glucose and lipid metabolism and improving insulin resistance. However, its underlying mechanisms of action remains unclear. Here, we demonstrate the protective effects and molecular mechanisms of action of CGA in reducing weight gain and hyperlipidemia in mice fed with a high‐fat diet (HFD). Methods and Results. C57BL/6 mice were fed with normal chow or HFD; half of the mice in each group received CGA treatment by oral gavage for 16 weeks. CGA treatment was found to significantly inhibit HFD‐induced weight gain and hyperlipidemia and increased energy expenditure by promoting the expression of genes involved in thermogenesis and mitochondrial biogenesis. Furthermore, CGA was shown to inhibit the enterohepatic farnesoid X receptor (FXR) fibroblast growth factor 15 (FGF15) pathway and changes serum bile acid (BA) pool, thereby contributing to the increased expression of cholesterol 7 α‐hydroxylase (CYP7A1). Conclusions. CGA increases the metabolic elimination of cholesterol by inhibiting the enterohepatic FXR/FGF15 pathway.

Adiponectin, an adipocyte-derived hormone with anti-inflammatory and antitumor activity, inhibits esophageal adenocarcinoma (EAC) cell proliferation and induces apoptosis. Chronic inflammation is a key process involved in initiation and progression of EAC, but the roles and mechanisms of adiponectin in inflammation have not been fully understood in EAC. We aimed to analyze the effects of two types of adiponectin, full-length adiponectin (f-Ad) and globular adiponectin (g-Ad), on inflammatory factors’ expression and explore the roles of ROS/NF-κB signaling pathway in adiponectin-regulated inflammation in EAC cells. It was found that f-Ad and g-Ad differently regulated both mRNA and protein levels of TNF-α, IL-8, and IL-6 in a dose-dependent manner in OE19 cells. g-Ad apparently induced TNF-α, IL-8, and IL-6 production, which was inhibited by PDTC or NAC, and increased intracellular ROS levels and NF-κB p65 activation, whereas f-Ad significantly suppressed production of inflammatory factors and NF-κB p65 activation and also decreased the intracellular ROS levels. In conclusion, the study demonstrated that g-Ad exerts a proinflammatory effect whereas f-Ad appears to induce an anti-inflammatory effect in a ROS/NF-κB-dependent manner in OE19 cells.