Disease relevance of beta-Penta-O-galloyl-glucose

• Pentagalloylglucose, which is found in many medicinal plants, can arrest the cell cycle at G(1) phase through down-regulation of cyclin-dependent kinases 2 and 4 and up-regulation of the cyclin-dependent kinase inhibitors p27(Kip1) and p21(Cip1/WAF1) in human breast cancer cells [1].
• In vitro anti-proliferative effect of 1,2,3,4,6-penta-O-galloyl-beta-D-glucose on human hepatocellular carcinoma cell line, SK-HEP-1 cells [2].
• The effects of pentagalloylglucose (1,2,3,4,6-penta-O-galloyl-beta-D-glucose) on the aerobic electron transport system of Escherichia coli were studied [3].
• In Vitro Antiviral Activity of 1,2,3,4,6-Penta-O-galloyl-beta-D-glucose against Hepatitis B Virus [4].

High impact information on beta-Penta-O-galloyl-glucose

• The turnover of p27(Kip1) and p21(Cip1/WAF1), which is necessary for cell cycle progression mediated by proteasome degradation, was disrupted by treatment of human Jurkat T cells with pentagalloylglucose [1].
• Induction of G1 arrest and apoptosis in human jurkat T cells by pentagalloylglucose through inhibiting proteasome activity and elevating p27Kip1, p21Cip1/WAF1, and Bax proteins [1].
• The addition of pentagalloylglucose to Jurkat T cells enhanced the stability of the proteasome substrate Bax and increased cytochrome c release and apoptosis [1].
• Pentagalloylglucose also induces apoptosis in human leukemic cells [1].
• Our findings suggest a mechanism for the effect of pentagalloylglucose on the cell cycle in human leukemic cells: that pentagalloylglucose down-regulates proteasome-mediated pathways because it is a proteasome inhibitor [1].

Biological context of beta-Penta-O-galloyl-glucose

• Induction of G1 phase arrest in MCF human breast cancer cells by pentagalloylglucose through the down-regulation of CDK4 and CDK2 activities and up-regulation of the CDK inhibitors p27(Kip) and p21(Cip) [5].
• Biosynthesis of gallotannins: formation of polygalloylglucoses by enzymatic acylation of 1,2,3,4,6-penta-O-galloylglucose [6].
• 1,2,3,4,6-Penta-O-galloyl-beta-D-glucose protects rat neuronal cells (Neuro 2A) from hydrogen peroxide-mediated cell death via the induction of heme oxygenase-1 [7].
• These findings suggest that pentagalloylglucose at low concentrations inhibits the electron transport system to decrease the RCR, but scarcely impairs the membrane, practically retaining the coupled reaction, while at high concentrations it impairs the structural integrity of the mitochondrial membrane [8].
• The IC50 of the compound for H+, K(+)-ATPase was 166 nmol/l. Kinetic analyses indicated that the inhibition of the enzyme by pentagalloylglucose was noncompetitive with respect to K+ [9].

Anatomical context of beta-Penta-O-galloyl-glucose

• Inhibition of the proteasome by pentagalloylglucose and by the proteasome inhibitor MG132 caused accumulation of ubiquitin-tagged proteins in Jurkat T cells [1].
• Pentagalloylglucose, hexagalloylglucose, heptagalloylglucose, and octagalloylglucose were extracted from PRE; they relaxed aortic rings with endothelium, but failed to relax aortic rings without endothelium [10].
• Immunohistochemical studies with antibodies raised against pentagalloylglucose and the galloyltransferase catalyzing the formation of this ester revealed that leaf mesophyll cell walls were a typical site of origin and deposition of hydrolyzable tannins [11].
• The respiratory control ratio (RCR) decreased by 50% on addition of 20 microM pentagalloylglucose to highly coupled mitochondria, but the adenosine-5'-diphosphate/oxygen (ADP/O) ratio decreased only slightly [8].
• The inhibitory effects of pure galloylglucose (1,2,3,4,6-penta-O-galloyl-beta-D-glucose) on the respiratory chain of rat liver mitochondria were investigated [8].

Associations of beta-Penta-O-galloyl-glucose with other chemical compounds

• An alpha-glucosidase inhibitor/antibiotic was purified from the freshwater green alga Spirogyra varians and was determined to be the pentagalloylglucose 3-O-digalloyl-1,2,6-trigalloylglucose [12].
• The contents of eight constituents (gallic acid, oxypaeoniflorin, albiflorin, paeoniflorin, benzoic acid, pentagalloylglucose, paeonol, and benzyoylalbiflorin) in these samples were determined by high-performance liquid chromatography [13].
• The activity of nicotineamide adenine dinucleotide (NADH) reductase was inhibited by pentagalloylglucose, but the activities of succinate dehydrogenase, D-lactate dehydrogenase, and ubiquinol-1 (Q1H2) oxidase were not susceptible to the inhibitor [3].
• In in vivo experiments, PGG was found to protect mice from a lethal challenge by LPS, and significantly decreased the plasma endotoxin level both in endotoxemic mice and rats, the reduction of the endotoxin level in rats being tightly associated with the TNF-alpha level [14].
• Combining SDS and native PAGE analyses showed instability in the macromolecular complexes formed from pentagalloylglucose (PGG) and BSA [15].

Gene context of beta-Penta-O-galloyl-glucose

• Pentagalloylglucose inhibits estrogen receptor alpha by lysosome-dependent depletion and modulates ErbB/PI3K/Akt pathway in human breast cancer MCF-7 cells [16].
• 1,2,3,4,6-penta-O-galloyl-beta-D-glucose up-regulates heme oxygenase-1 expression by stimulating Nrf2 nuclear translocation in an extracellular signal-regulated kinase-dependent manner in HepG2 cells [17].
• 1,2,3,4,6-Penta-O-galloyl-beta-D-glucose blocks endothelial cell growth and tube formation through inhibition of VEGF binding to VEGF receptor [18].
• Inhibition of inducible nitric oxide synthase and cyclooxygenase-2 activity by 1,2,3,4,6-penta-O-galloyl-beta-D-glucose in murine macrophage cells [19].
• We now show that pentagalloylglucose inhibits the activities of purified 20 and 26 S proteasomes in vitro, the 26 S proteasome in Jurkat T cell lysates, and chymotrypsin-like activity of the 26 S proteasome in intact Jurkat T cells [1].

Analytical, diagnostic and therapeutic context of beta-Penta-O-galloyl-glucose

• The CZE method was used to determine the content of paeonol, oxypaeoniflorin, benzoic acid, pentagalloylglucose and gallic acid, and MEKC technique based on sodium cholate was applied to analyze albiflorin, paeoniflorin, benzoyla biflorin, paeonol and oxypaeoniflorin [20].
• The water extract of peony roots, albiflorin and pentagalloylglucose given orally completely inhibited the EEG power spectrum changes as well as the extracellular calcium and potassium concentration changes related to seizure activity [21].
• After preparation using standard methods, including silica gel chromatography and HPLC, we obtained 1, 2, 3, 4, 6-beta-d-pentagalloylglucose (PGG), with lipid A-binding ability [14].

References