The study was undertaken to determine whether low dose of endotoxin could induce rat brain damage, and its relation to the metabolism of oxygen free radicals. Male Wistar rats were treated with E. Coli endotoxin intraperitoneally (2 mg/kg body wt). Fourteen hours later, the lipoperoxide level was markedly elevated in animals given endotoxin compared with that in the controls (5.0?1.0 vs 3.9?0.7, P

A BASIC program was written to analyse the data from radioreceptor assay by microcomputer. Concentrations of ligand, total binding, nonspecific binding, specific binding and the ratio of specific binding (number of receptor sites) to free ligand content were calculated for each point. The receptor binding affinity constant and binding capacity were obtained by Sca-tchard analysis. Results and graphs can be displayed on the screen and/ or printed out by using a graphic printer

Objective:To identify key genes and their potential biological mechanisms in the progression of non-alcoholic fatty liver disease (NAFLD) using bioinformatics technology.Methods:Genes differentially expressed in simple non-alcoholic fatty liver disease (NAFL) and non-alcoholic steatohepatitis (NASH) were analyzed by integrating NAFLD-related sequencing datasets GSE135251 and GSE167523 from the Gene Expression Omnibus (GEO) datebase. Gene Ontology (GO) functional enrichment analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) and Reactome signaling pathway analysis were performed. Key genes were identified by STRING database and Cytoscape3.7.2 software, and the expression of key genes under different fibrosis grades and activity scores was observed. In addition, the expression of key genes in different cell clusters was observed based on the single-cell RNA-seq dataset of NAFLD mice.Results:Bioinformatics methods were used to obtain 97 common differential genes in NAFLD from two datasets. GO functional enrichment analysis was mainly performed in Extracellular Matrix (ECM) tissues. The main signaling pathway is ECM-receptor interaction. Five key genes were identified based on PPI network and Cytoscape software: COL1A1, THBS2, CXCL8, THY1 and LOXL1. The expression of key genes was significantly positively correlated with fibrosis grade and activity score, indicating that they were closely related to the progression of NAFLD. These key genes are highly expressed in hepatic stellate cells (HSCs) and natural killer/T cells (NK/T cells).Conclusion:In this study, bioinformatics technology was used to identify five key genes that may be involved in the NAFL-NASH transformation, suggesting that the ECM-receptor interaction signaling pathway may be a key molecular mechanism of NAFLD disease progression.