Ontology highlight
ABSTRACT:
PROVIDER: PRJNA853465 | ENA |
REPOSITORIES: ENA
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Project description:Hawk tea (Litsea coreana var. lanuginose) is a traditional Chinese tea, widely cultivated and consumed in southwestern China. It has been widely used to treat gastrosis, hepatitis, and inflammatory diseases for hundreds of years. Modern pharmacological studies demonstrate that hawk tea has protective effects against liver fibrosis, hypercholesterolemia, hyperglycemia, and inflammatory diseases . However, the molecular mechanism of hawk tea against hypercholesterolemia remains unclear. The aims of this study were to investigate the mechanisms of hawk tea extract (HTE) to lower cholesterol. Therefore, we performed genome-wide transcriptional analysis of hawk tea extracts treated HepG2 cells. Hawk tea extracts (HTE) induced significant gene modulation on HepG2 cells.
2018-07-25 | GSE117583 | GEO
Project description:Hawk tea (Litsea coreana var. lanuginose) is a traditional Chinese tea, widely cultivated and consumed in southwestern China. It has been widely used to treat gastrosis, hepatitis, and inflammatory diseases for hundreds of years. Modern pharmacological studies demonstrate that hawk tea has protective effects against liver fibrosis, hypercholesterolemia, hyperglycemia, and inflammatory diseases . However, the molecular mechanism of hawk tea against hypercholesterolemia remains unclear. The aims of this study were to investigate the mechanisms of hawk tea extract (HTE) to lower cholesterol. Therefore, we performed genome-wide transcriptional analysis of hawk tea extracts treated HepG2 cells.
2017-12-10 | GSE107879 | GEO
Project description:Di (2-ethylhexyl) phthalate (DEHP) is a common plasticizer. Studies have revealed that DEHP exposure can cause liver damage. Green tea is one of the most popular beverages in China. Green tea polyphenols (GTPs) have been proven to have therapeutic effects on organ damage induced by heavy metal exposure. However, few study report on GTP relieving DEHP-induced liver damage.
2023-10-03 | GSE232128 | GEO
Project description:Growth inhibition of the pathogen Staphylococcus aureus with currently available antibiotics is problematic in part due to bacterial biofilm protection. While Although the recently characterized natural products, including 3´,4´,5-trihydroxy-6,7-dimethoxy-flavone [1], 3´,4´,5,6,7-pentahydroxy-flavone [2] and 5-hydroxy-4´,7-dimethoxy-flavone [3] exhibit both antibiotic and biofilm inhibitory activities, the mode of action of such hydroxylated flavonoids with respect to S. aureus inhibition has is yet to be characterized. Enzymatic digestion and high- resolution MS mass spectral analysis of differentially expressed proteins from S. aureus, with and without exposure to antibiotic flavonoids (1-3) has allowed for the characterization of global -protein alterations induced by metabolite treatment. A total of 56, 92, and 110 proteins are were differentially expressed with bacterial exposure to 1, 2 or 3, respectively. Connectivity of identified proteins is characterized using a search tool for the retrieval of interacting genes/proteins (STRING) with multi-targeted S. aureus inhibition of energy metabolism and biosynthesis by the assayed flavonoids observed. Identifying the mode of action of natural products as antibacterial agents is expected to provide insight into the potential use of flavonoids alone or in combination with known therapeutic agents to effectively control S. aureus infection.
2017-05-30 | PXD006030 | Pride
Project description:Background and aims: Signal transducer and activator of transcription 3 (Stat3) is the main mediator of interleukin-6 type cytokine signaling required for hepatocyte proliferation and hepatoprotection but its role in sclerosing cholangitis and other cholestatic liver diseases remains unresolved. Methods: We investigated the role of Stat3 in inflammation-induced cholestatic liver injury and used mice lacking the multidrug resistance gene 2 (mdr2-/-) as a model for SC. Results: We demonstrate that conditional inactivation of stat3 in hepatocytes and cholangiocytes (stat3 delta hc) of mdr2-/- mice strongly aggravated bile acid-induced liver injury and fibrosis. A similar phenotype was observed in mdr2-/- mice lacking IL-6 production. Biochemical and molecular characterization suggested that Stat3 exerts hepatoprotective functions in both, hepatocytes and cholangiocytes. Loss of Stat3 in cholangiocytes led to increased expression of TNFα which might reduce the barrier function of bile ducts. Loss of Stat3 in hepatocytes led to upregulation of bile acid biosynthesis genes and downregulation of hepatoprotective epidermal growth factor receptor and insulin-like growth factor 1 signaling pathways. Consistently, stat3deltahc mice were more sensitive to cholic acid-induced liver damage than control mice. Conclusions: Our data suggest that Stat3 prevents cholestasis and liver damage in sclerosing cholangitis via regulation of pivotal functions in hepatocytes and cholangiocytes. Affymetrix microarray analyses was performed to identify metabolic and molecular pathways in stat3Dhc mdr2-/- mice that lead to cholestasis and bile acid-induced liver injury. To avoid false positive results that are due to differential cellular composition, we defined the onset of fibrosis and expression of fibrogenic factors in stat3Dhc mdr2-/- mice.
2010-10-20 | E-GEOD-18759 | biostudies-arrayexpress
Project description:To further investigate the potential molecular basis of the therapeutic effects of the mixture of salvianolic acids from Salvia miltiorrhiza and total flavonoids from Anemarrhena asphodeloides (MSTF) on sulfur mustard (SM) damage, gene expression analysis was conducted on rats liver tissues using microarrays.
2014-11-05 | GSE62994 | GEO
Project description:The high-fat diet (HFD)-feeding significantly stimulated hypercholesterolemia in male SD rats. Simultaneous feeding of hawk tea extracts (HTE) reversed the hypercholesterolemia in rats by lowering the serum total cholesterol and low-density lipoprotein cholesterol levels. To understand the molecular mechanism underlying the cholesterol-lowering effects of HTE, we performed the RNA-seq analysis. Consequently, the change in mRNA levels of genes invovled in metabolism of lipid and lipoprotein, primary bile acid synthesis, and ABC transporters itriggered by HFD-feeding were reversed by the co-administration of HTE (200 mg/kg/day for 11 weeks).
2019-05-21 | GSE125084 | GEO
Project description:Smilax glabra Roxb, a traditional Chinese herb, has been widely used for folk medicine. Previous studies have found that it has various pharmacological activities, such as cytotoxic, anti-inflammation, anti-oxidant, hepatoprotective, and cardiovascular system protective activities. However, its roles in adipogenesis are poorly understood. We hypothesized that Smilax glabra Roxb and its main component may play important roles in regulating adipocyte diffrentiation and function. To test this hypothesis, we performed RNA-Seq on 3T3-L1 adipocytes treated with and without pure total flavonoids from Smilax glabra Roxb.
2022-01-11 | GSE124950 | GEO
Project description:Mouse models of acute and chronic liver damage
| PRJNA702143 | ENA
Project description:Acute liver injury is a critical life-threatening event. Common causes are infections, intoxication, and ischemic conditions. The cytokine Interleukin 22 (IL-22) has been implicated in this process. However, the role of IL-22 during acute liver damage is controversial, since both protective and pathogenic properties have been reported. IL-22 binding protein (IL-22BP, IL-22Ra2), a soluble endogenous inhibitor of IL-22, is able to regulate IL-22 activity, and thus might explain some of the controversial findings. Since the role of IL-22BP in liver injury is unknown, we used Il22bp deficient mice and mouse models for acute liver damage to address this point. We found that Il22bp deficient mice were more susceptible to ischemia- and acetaminophen- induced liver damage. Deficiency of Il22bp caused increased hepatic damage and delayed liver regeneration. Using an unbiased approach, we found that IL-22, if uncontrolled in Il22bp deficient mice, induced Cxcl10 expression by hepatocytes, thereby recruiting inflammatory CD11b+Ly6C+ monocytes into the liver upon liver damage. Accordingly, neutralization of Cxcl10 reversed the increased disease susceptibility of Il22bp deficient mice. In conclusion, our data suggest dual functions of IL-22 in acute liver damage, and highlight the need to control IL-22 activity via IL-22BP.
2017-12-22 | GSE93034 | GEO