Project description:To explore the regulatory mechanism of intestinal flora in Citrobacter rodentium -induced intestinal infection by transcriptome analysis at miRNA molecular level.
Project description:The relative quantification of sex-specific proteomic responses led to the detection of potential biomarkers for hepatotoxicity and as well as the identification of the underlying molecular perturbation needed to unravel the impact of APAP-induced liver injury on physiological system.
Project description:Drosophila melanogaster was used to investigate the influence of microbiota-derived intestinal flora and its metabolites on host transcriptional regulation by adding sodium butyrate to a sterile diet for constructing a sterile Drosophila model. In order to further investigate the effects of sodium butyrate on Drosophila melanogaster at the molecular mechanism level, we detected the abundance and composition of midgut microbial colonies based on 16S rRNA gene sequences, and analyzed the overall structure and metabolic activities of host transcriptional networks by combining transcriptome and non-target metabolomics data.
Project description:Acute liver failure is a serious clinical manifestation resulting from sudden liver injury, which can be triggered by various factors. One of the most frequent causes of acute liver failure is excessive ingestion of acetaminophen (APAP), which is known to damage hepatocytes directly by reducing glutathione levels in cells, ultimately leading to hepatocyte death.PGE2 can play a dual role in inflammation, either promoting or inhibiting the inflammatory response, depending on the cell type, local concentration, receptor type, and tissue microenvironment. Early studies have shown that PGE2 significantly alleviated acute liver failure induced by galactosamine/lipopolysaccharide, APAP, and carbon tetrachloride. However, the precise mechanism by which PGE2 alleviates APAP-induced acute liver failure remains unclear. The aim of this study is to investigate the mechanisms underlying the protective effects of PGE2 against APAP-induced hepatocyte injury.
Project description:Acute liver failure is a serious clinical manifestation resulting from sudden liver injury, which can be triggered by various factors. One of the most frequent causes of acute liver failure is excessive ingestion of acetaminophen (APAP), which is known to damage hepatocytes directly by reducing glutathione levels in cells, ultimately leading to hepatocyte death.PGE2 can play a dual role in inflammation, either promoting or inhibiting the inflammatory response, depending on the cell type, local concentration, receptor type, and tissue microenvironment. Early studies have shown that PGE2 significantly alleviated acute liver failure induced by galactosamine/lipopolysaccharide, APAP, and carbon tetrachloride. However, the precise mechanism by which PGE2 alleviates APAP-induced acute liver failure remains unclear. The aim of this study is to investigate the mechanisms underlying the protective effects of PGE2 against APAP-induced hepatocyte injury.
Project description:Acute liver failure is a serious clinical manifestation resulting from sudden liver injury, which can be triggered by various factors. One of the most frequent causes of acute liver failure is excessive ingestion of acetaminophen (APAP), which is known to damage hepatocytes directly by reducing glutathione levels in cells, ultimately leading to hepatocyte death.PGE2 can play a dual role in inflammation, either promoting or inhibiting the inflammatory response, depending on the cell type, local concentration, receptor type, and tissue microenvironment. Early studies have shown that PGE2 significantly alleviated acute liver failure induced by galactosamine/lipopolysaccharide, APAP, and carbon tetrachloride. However, the precise mechanism by which PGE2 alleviates APAP-induced acute liver failure remains unclear. The aim of this study is to investigate the mechanisms underlying the protective effects of PGE2 against APAP-induced hepatocyte injury.
Project description:Intestinal ischemia-reperfusion (IR) injury is associated with high mortality rates, which have not improved in the past decades despite advanced insight in its pathophysiology using in vivo animal and human models. The inability to translate previous findings to effective therapies emphasizes the need for a physiologically relevant in vitro model to thoroughly investigate mechanisms of IR-induced epithelial injury and test potential therapies. In this study, we demonstrate the use of human small intestinal organoids to model IR injury by exposing organoids to hypoxia and reoxygenation (HR). A mass-spectrometry-based proteomics approach was applied to characterize organoid differentiation and decipher protein dynamics and molecular mechanisms of IR injury in crypt-like and villus-like human intestinal organoids.
Project description:Acetaminophen (APAP) is the most widely used analgesic in the United States. Its acute overdose causes liver damage by inducing localized centrilobular cell death. Because of widespread use, APAP toxicity has become the most frequent cause of acute liver failure. Many factors have been associated with the susceptibility of APAP-induced liver injuries, however, few of them have been confirmed and used in the clinical setting. We tried to identify the subset of factors that could affect susceptibility to APAP-induced liver injury by an integrative genetic, transcriptional and 2-D-NMR-based metabolomic analysis across a panel of inbred mouse strains. Experiment Overall Design: After a single administration of high dose (300 mg/kg i.p.) APAP, liver and blood samples were extracted from 3 sensitive (C57B6, DBA/2, and SmJ) and 1 resistant (SJL) mice strains at 0, 3 and 6 hour after APAP exposure. Endogenous metabolites from liver samples were analyzed by 1H-13C 2-dimensional-NMR and gene expression changes occurring within these liver samples were simultaneously analyzed using Affymetrix microarrays. The transcriptional and metabolomic data was jointly analyzed, and functional information within the Gene Ontology database was used to identify the subset of genes that could affect susceptibility to APAP-induced liver injury in the early phase response.
Project description:Acute liver failure is a serious clinical manifestation resulting from sudden liver injury, which can be triggered by various factors. Early studies have shown that PGE2 significantly alleviated acute liver failure induced by galactosamine/lipopolysaccharide(Dgaln/lps), APAP, and carbon tetrachloride. However, the precise mechanism by which PGE2 alleviates Dgaln/lps-induced acute liver failure remains unclear. The aim of this study is to investigate the mechanisms underlying the protective effects of PGE2 against Dgaln/lps-induced hepatocyte injury.
