Identification of hub genes, signaling pathways and immune infiltration of recurrent spontaneous abortion based on bioinformatics analysis with clinical verification.

OBJECTIVE: The present study was aimed to identify hub genes associated with recurrent spontaneous abortion (RSA) via both bioinformatics analysis and clinical verification, also to evaluate the related pathways and immune infiltration situation of RSA, for exploring its underlying mechanism. MATERIALS AND METHODS: We screened candidate hub genes associated with RSA via bioinformatic analysis in the microarray datasets GSE22490 downloaded from the Gene Expression Omnibus (GEO) database. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Western blotting were used to validate these hub genes. Several kinds of enrichment analysis were carried out to find out the pathways related to RSA. Additionally, CIBERSORT was used for evaluation of local immune Infiltration status of RSA. RESULTS: There were 536 differentially expressed genes (DEGs) including 301 upregulated and 235 downregulated genes in RSA group compared with healthy control group. Four hub genes (STAT3, TLR2, TLR4 and CD86) were finally screened out according to the protein-protein interaction (PPI) network analysis, RT-qPCR and Western blotting. Enrichment analysis showed that Toll-like receptor signaling pathway, neutrophil chemotaxis, chemokine signaling pathway and Fc gamma receptor-mediated phagocytosis were strongly associated with RSA. And in immune infiltration analysis, RSA tissue was found containing a higher proportion of monocytes and eosinophils. CONCLUSION: This study screened out four hub genes and several important pathways changed in the trophoblastic tissue of RSA patients. We also found that monocytes and eosinophils may be involved in RSA. These findings provide theoretical basis for further studies on the mechanisms of RSA.

Benzophenones from Guignardia sp. IFB-E028, an endophyte on Hopea hainanensis.

The first natural S-containing benzophenone dimer, named guignasulfide (3), was isolated from the culture of Guignardia sp. IFB-E028, an endophytic fungus residing in healthy leaves of Hopea hainanensis. Its structure was determined through correlative analyses of its MS, 1D- and 2D-NMR spectroscopic data. Two other known benzophenone derivatives, monomethylsulochrin and rhizoctonic acid (1 and 2, resp.) were also isolated. Guignasulfide (3) was more active against the human liver cancer cell line HepG2 (IC(50) value: 5.2+/-0.4 microM) than metabolites 1 and 2 (IC(50) values: 63.5+/-0.6 and 60.2+/-0.5 microM); compounds 1-3 showed also moderately inhibitory effects on the human bacterial pathogen Helicobacter pylori with MIC values of 28.9+/-0.1, 60.2+/-0.4, and 42.9+/-0.5 microM, respectively.

Inhibition of soluble epoxide hydrolase by extracts derived from inflammation-treating Chinese medicinal herbs.

Soluble epoxide hydrolase (sEH) has been proved to be a key enzyme involved in inflammation progression, and inhibition of sEH is therefore very helpful or crucial for the treatment of inflammation-related diseases. In order to uncover new clues suggesting the presence of phytochemical-based sEH inhibitors, and to rationalize the utility of the inflammation-treating Chinese medicinal herbs, the ethanol extracts derived from 46 medicinal herbs, traditionally used for the treatment of inflammation-associated diseases in China, were tested for sEH-inhibition activity using a recently developed sensitive fluorescence-based assay. Screened at 10 microg/mL, four extracts showed substantial inhibitions of sEH (inhibition rates >50%). The ethanol extract of Sophora flavescens root (Fabaceae) possessed the strongest inhibitory activity against sEH (IC(50): 2.07 microg/mL). These preliminary findings highlighted the presence of sEH inhibitor(s) in the plant kingdom, and the possibility that the inflammation-treating herbal medicines could be an untapped reservoir for sEH-inhibition agents.

Synthesis and cytotoxic evaluation of a series of genistein derivatives.

Thirty genistein (= 5,7-dihydroxy-3-(4-hydroxyphenyl)-4H-1-benzopyran-4-one; GEN) derivatives were synthesized from genistein through a facile approach in high yields. Compounds 9, 11, 12, 23-30 were reported for the first time, while 13-22 have already been reported in our recent paper. The cytotoxic activities of these compounds were evaluated against a human nasopharyngeal epidermoid tumor cell line KB. Compounds 7-9, 12, 14, 16-19, 21, 24, 27, 29 showed remarkable antitumor activities in vitro, which was comparable with 5-fluorouracil, an anticancer drug. On the basis of the obtained experimental data, structure-effect relationships were discussed.

The therapeutic effects of tectorigenin on chemically induced liver fibrosis in rats and an associated metabonomic investigation.

The aim of this study was to investigate the effects of tectorigenin on chemically induced liver fibrosis in rats. Liver fibrosis was induced in rats with carbon tetrachloride, a diet high in fat, cholesterol and alcohol in the drinking water. Our results indicate that tectorigenin treatment significantly inhibited the increases in the activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and the increases in the serum levels of hyaluronate (HA), laminin (LN) and procollagen III N-terminal peptide (PIIIP); tectorigenin treatment also significantly inhibited the increases in the amount of collagen in the livers of the fibrogenic rats. Chemically induced liver fibrosis caused a drop in the serum albumin concentration and a decrease in the ratio of albumin to globulin (A/G). Tectorigenin caused a remarkable increase at a dose of 30 mg/kg, but only a slight increase at the lower doses. Tectorigenin was also able to inhibit the increase in the liver lipid peroxidation (LPO), as well as the decrease in the activities of liver superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), caused by liver fibrosis. In addition, we present a related metabolic profile determined, using a (1)H NMR spectroscopy and multivariate pattern recognition techniques. The results were consistent with the pathological examination, liver function analysis and liver fibrosis marker analysis. Furthermore, tectorigenin does not cause acute toxicity.