Disease relevance of C10462

• Pharmacokinetics of [6]-gingerol after intravenous administration in rats with acute renal or hepatic failure [1].
• [6]-Gingerol Induces Cell Cycle Arrest and Cell Death of Mutant p53-expressing Pancreatic Cancer Cells [2].
• [6]-Gingerol (50 mg/kg-100 mg/kg) also produced an inhibition of paw edema induced by carrageenin [3].

High impact information on C10462

• Inhibition of epidermal growth factor-induced cell transformation and activator protein 1 activation by [6]-gingerol [4].
• In our present study, topical application of [6]-gingerol inhibited COX-2 expression in mouse skin stimulated with a prototype tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) [5].
• Moreover, [6]-gingerol prevented TPA-induced phosphorylation and catalytic activity of p38 mitogen-activated protein (MAP) kinase that regulates COX-2 expression in mouse skin [5].
• [6]-Gingerol inhibits COX-2 expression by blocking the activation of p38 MAP kinase and NF-kappaB in phorbol ester-stimulated mouse skin [5].
• Phosphorylation of both IkappaBalpha and p65 was substantially blocked by [6]-gingerol [5].

Biological context of C10462

• In vitro, [6]-gingerol inhibited both the VEGF- and bFGF-induced proliferation of human endothelial cells and caused cell cycle arrest in the G1 phase [6].
• The active part of the [6]-gingerol molecule in mutagenesis [7].
• Kinetics of [6]-gingerol degradation was characterized by least square fitting of a rate equation [8].
• Pharmacokinetics of [6]-gingerol after intravenous administration in rats [9].
• Microsomal hydroxylation and glucuronidation of [6]-gingerol [10].

Anatomical context of C10462

• Hepatic microsomes from rats and humans fortified with UDPGA glucuronidated [6]-gingerol predominantly at the phenolic hydroxyl group, but small amounts of a second monoglucuronide involving the aliphatic hydroxyl group were also identified by LC-MS/MS analysis [10].
• Induction of apoptosis in HL-60 cells by pungent vanilloids, [6]-gingerol and [6]-paradol [11].
• In this study, the effect of [6]-gingerol, a pungent phenolic compound present in ginger (Zingiber officinale Roscoe), on NO synthesis in lipopolysaccharide (LPS)-activated J774.1 macrophages was tested, and the protective ability of this compound against peroxynitrite-mediated oxidation and nitration reactions were evaluated [12].
• It is reported that resiniferatoxin, [6]-gingerol and lafutidine are compounds that activate VR1 and/or capsaicin-sensitive afferent neurons [13].
• Addition of 30 and 100 microM [6]-gingerol (a pungent constituent of ginger) induced contraction of the ileum immediately [14].

Associations of C10462 with other chemical compounds

• 2. [6]-Gingerol and [8]-gingerol evoked capsaicin-like intracellular Ca(2+) transients and ion currents in cultured DRG neurones [15].
• Ginger (Zingiber officinale Roscoe, Zingiberaceae) contains such pungent ingredients as [6]-gingerol and [6]-paradol, which also have anti-tumor promotional and antiproliferative effects [16].
• In order to discover the mechanism of inhibition, [6]-gingerol was reacted with peroxynitrite and the reaction mixture was analyzed using HPLC [17].
• Quantitative measurements of [6]-gingerol and its major degradation product [6]-shogaol [1-(4-hydroxy-3-methoxyphenyl)decan-4-ene-3-one] were performed by HPLC [8].
• It was observed that the combination of plant derived molluscicide and their active molluscicidal components, viz. tigogenin, hecogenin, azadirachtin, allicin, thymol, and [6]-gingerol combination with MGK-264 or piperonyl butoxide caused a significant reduction in fecundity, hatchability, and survival of young snails [18].

Gene context of C10462

• Western blot analyses indicated that [6]-gingerol decreased both Cyclin A and Cyclin-dependent kinase (Cdk) expression [2].
• In addition, [6]-gingerol inhibited TPA-stimulated interaction of phospho-p65-(Ser-536) with cAMP response element binding protein-binding protein, a transcriptional coactivator of NF-kappaB [5].
• Previous studies have demonstrated that [6]-gingerol inhibits mouse skin tumor promotion and anchorage-independent growth of cultured mouse epidermal cells stimulated with epidermal growth factor [19].
• Taken together, our data suggest that [6]-gingerol inhibits TPA-induced COX-2 expression in mouse skin in vivo by blocking the p38 MAP kinase-NF-kappaB signaling pathway [5].
• Inhibitory effects of [6]-gingerol, a major pungent principle of ginger, on phorbol ester-induced inflammation, epidermal ornithine decarboxylase activity and skin tumor promotion in ICR mice [20].

Analytical, diagnostic and therapeutic context of C10462

• The total cumulative amount of 1 excreted in the bile and 2-7 in the urine during 60 h after the oral administration of [6]-gingerol were approximately 48% and 16% of the dose, respectively [21].
• [6]-Shogaol and [6]-gingerol, known neutral components of ginger rhizomes, were detected using gas chromatography and were found to be the most prevalent components in the fraction, occurring in quantities that resulted in a dose-dependent killing efficacy [22].
• These results suggest that [6]-gingerol can circumvent the resistance of mutant p53- expressing cells towards chemotherapy by inducing apoptotic cell death while it exerts cytostatic effect on wild type p53- expressing cells by inducing temporal growth arrest [2].

References