“Quercetin has been shown to act as an anticarcinogen
in experimental colorectal cancer (CRC). The aim of the present study was to characterize transcriptome and proteome changes occurring in the distal colon mucosa of rats supplemented with 10 g quercetin/kg diet for 11 wk. Transcriptome data analyzed with Gene Set Enrichment Analysis showed that quercetin significantly downregulated the potentially oncogenic mitogen-activated protein kinase (Mapk) pathway. In addition, quercetin enhanced expression of tumor suppressor genes, including Pten, Tp53, and Msh2, and of https://www.selleckchem.com/products/bay-57-1293.html cell cycle inhibitors, including Mutyh. Furthermore, dietary quercetin enhanced genes involved in phase I and II metabolism, including Fmo5, Ephx1, Ephx2, and Gpx2. Quercetin increased PPAR alpha target genes, and concomitantly enhanced expression of genes involved in mitochondrial fatty acid (FA) degradation. Proteomics performed in the same samples revealed 33 affected proteins, of which four glycolysis selleck enzymes and three heat shock proteins
were decreased. A proteome-transcriptome comparison showed a low correlation, but both pointed out toward altered energy metabolism. In conclusion, transcriptomics combined with proteomics showed that dietary quercetin evoked changes contrary to those found in colorectal carcinogenesis. These tumor-protective mechanisms were associated with a shift in energy production pathways, pointing at decreased cytoplasmic glycolysis and toward
increased mitochondrial FA degradation.”
“Pregnant rats were treated daily with 1 g/L of L-glutamate in Methylitaconate Delta-isomerase their drinking water during pregnancy and/or lactation. The effect on adenosine A, receptor (A,R) and A(2A) receptor (A R) in brains from both mothers and 15-day-old neonates was assayed using radioligand binding and real time PCR assays. Mothers receiving L-glutamate during gestation, lactation, and throughout gestation and lactation showed a significant decrease in total A(1)R number (water+water, 302+/-49 fmol/mg; L-glutamate+water, 109+/-11 fmol/mg, P<0.01; water+L-glutamate, 52 13 fmol/mg, P<0.01; L-glutamate+L-glutamate, 128+/-33 fmol/mg, P<0.05). No variations were detected in the Kd parameter. Concerning adenosine A R, radioligand binding assays revealed that Bmax parameter remains unaltered in maternal brain in response to glutamate exposure. However, Kd parameter was significantly decreased in all L-glutamate-treated groups (water+water, 5.3+/-1.3 nM; L-glutamate water, 0.5+/-0.1 nM; water+L-glutamate, 0.9+/-0.1 nM; L-glutamate L-glutamate, 0.7+/-0.1 nM, P<0.01 in all cases).