Microarray Expression Profiling of Punicalagin, Myricetin and Quercetin Treated Leukemia Cell Line (THP-1)
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PROVIDER: PRJNA673188 | ENA |
REPOSITORIES: ENA
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Project description:THP-1 monocyte were differentiated to macrophage using PMA for 24 hrs, then (THP-1) macrophage were treated with DMSO, Punicalagin, Myricetin or Quercetin for 24 hrs. Transcriptional expression profiling was performed with Affymetrix GeneChips. Target preparation, hybridization, washing and staining, and probe array scanning were done to process array.
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Project description:In order to identify patterns of gene expression associated with biological effects in THP-1 cells induced by F3, we performed a transcriptomic analysis on the THP-1 control and F3-treated THP-1 cells by oligonucleotide microarray Experiment Overall Design: 10^7 cells/mL concentrations of THP-1 cells were seeded in 100 mm dish and incubated overnight. After that, cells were treated with F3 at a final concentration of 30 ug/mL. After incubated for 6 and 24 hours, the cell pellets were collected by centrifugation at 250g for 5 min, correspondingly. Controlled samples of un-induced cells were treated in the same way with the same amount of medium.
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Project description:Quercetin is a food component that may ameliorate the diabetic symptoms. We examined hepatic gene expression of BALB/c mice with streptozotocin (STZ)-induced diabetes to elucidate the mechanism of the protective effect of dietary quercetin on diabetes-associated liver injury. We fed STZ-induced diabetic mice with diets containing 0.1% or 0.5% quercetin for 2 weeks and compared the patterns of hepatic gene expression in these groups of mice using a DNA microarray. Diets containing 0.1% or 0.5% quercetin lowered the STZ-induced increase in blood glucose levels and improved plasma insulin levels. A cluster analysis of the hepatic gene expressions showed that 0.5% quercetin diet suppressed STZ-induced alteration of gene expression. Gene set enrichment analysis (GSEA) and quantitative RT-PCR analysis showed that the quercetin diets had their greatest suppressive effect on the STZ-induced elevation of expression of cyclin dependent kinase inhibitor p21(WAF1/Cip1) (Cdkn1a).
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Project description:As the critical step of pathogenesis during hypoxic pulmonary arterial hypertension (PAH) vascular remodeling is closely associated with pulmonary arterial smooth muscle cell (PASMC) alterations induced by hypoxia that include persistent vasoconstriction, abnormal proliferation and PASMC resistance to apoptosis. Quercetin is a flavonoid compound extracted from green plants that inhibits proliferation, induces apoptosis, arrests the cell cycle, and rescues the constriction of PASMCs, but the underlying mechanisms remain poorly understood. In this study, we used a commercial Agilent Whole Rat Genome Oligo Microarray to determine the overall transcriptional response of PASMCs in response to exposure to hypoxia and the optimal concentration of quercetin. Hypoxia induced the upregulation of 1694 genes and the downregulation of 2091 genes compared with the normoxia group. Quercetin treatment resulted in 1790 upregulated genes and 1450 downregulated genes. Quercetin is known to cause differential expression of several of these genes that are known to promote proliferation, induce apoptosis (Cycs, Ppp3ca, Prkar2b, Akt3, Ppp3cc, Il1rap, Ntrk1), arrest the cell cycle (Chek2, Cdkn1c, Gadd45b, Stag2, Anapc7, Orc1, Ccne1, Myc3, Skp1, Espl1, Cdc45, Mcm4), and rescue PASMC constriction (Ramp1, Ramp3, Adcy5, Gnas, Prkcd, Itpr3, Adra1d, Calm1, Npr1, Avpr1a, Ednra, Adcy8). Real-time quantitative RT-PCR was performed to verify the microarray results. In conclusion, quercetin altered the expression profile of many genes regulated by hypoxia in PASMCs, which helps to further explore the mechanism of the effects of quercetin treatment on hypoxic PAH.
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Project description:Differential gene expression in mice liver after Quercetin administration. Gene expression from control mice were compared with Quercetin treated mice at different dose level 2-color experiment. The normalization was done using channel split method as biological replicates were hybridized to the same microarray.
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Project description:Given the positive results of quercetin in in vitro genotoxicity studies, it is of interest to test the in vivo genotoxicity of this important dietary flavonoid, especially considering possible high intake by widely available supplements. In the present study quercetin was tested in a transcriptomic analysis for genotoxicity in liver and small intestine of mice. Quercetin (0.33%) supplemented to a high-fat diet was administered to mice during 12 weeks and compared with high-fat diet feeding. Serum ALT and AST levels revealed no indications for hepatotoxicity. General microarray pathway analysis of liver and small intestinal tissue samples showed no regulation of genotoxicity related pathways. In addition, analysis of DNA damage pathways in these samples, also did not point at genotoxicity. Furthermore, comparison with a published classifier set of transcripts for identifying genotoxic compounds did not reveal any similarities with the regulation of these classifier set of transcripts by quercetin, except for two of the transcripts which were regulated in opposite direction. Available microarray datasets of known genotoxic compounds, 2-acetylaminofluorene (2-AAF) and aflatoxin B1 (AFB1) in mice were taken along as positive controls for comparison, and indeed showed genotoxic properties (regulation of genotoxic related genes) in the analyses. This transcriptomic study showed that supplementation with quercetin at ~350 mg/kg bw/day for 12 weeks in mice gave no indications of quercetin-induced genotoxicity in liver and small intestine.
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