In vitro and In vivo inhibition of LPS-stimulated tumor necrosis factor-α secretion by the gallotannin β- d -pentagalloylglucose

Feldman, Ken S.; Sahasrabudhe, Kiran; Lawlor, Michael D.; Wilson, Sarah L.; Lang, Charles H.; Scheuchenzuber, William J.

doi:10.1016/s0960-894x(01)00332-8

Cited by 63 publications

(46 citation statements)

References 11 publications

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“…Day zero on the graph is day 7 after tumor injection. *Denotes significant differences (p < 0.05) with respect to control (days [3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19], † significant with respect to prevention group at day 14. (B) Real time pCR analysis of TNFα, IL-1α and IL6 in the tumor tissue sections of control and GT-treated mice.…”

Section: Discussionmentioning

confidence: 99%

Gallotannin inhibits NFĸB signaling and growth of human colon cancer xenografts

Al-Halabi¹,

Chedid²,

Merhi³

et al. 2011

Cancer Biology & Therapy

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Section: Discussionmentioning

confidence: 99%

Gallotannin inhibits NFĸB signaling and growth of human colon cancer xenografts

Al-Halabi¹,

Chedid²,

Merhi³

et al. 2011

Cancer Biology & Therapy

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Section: Introductionmentioning

confidence: 99%

“…Gallotannin and other tannins have been shown to exert various biological effects ranging from anti-inflammatory to anticancer and antiviral effects (Fong et al, 1972;Mota et al, 1985;Uchiumi et al, 1996;Van Molle et al, 2000;Feldman et al, 2001). The mechanisms underlying the anti-inflammatory effect of tannins include the scavenging of radicals (antioxidant effect) (Hagerman et al, 1999) and inhibition of the expression of inflammatory mediators, such as some cytokines (Feldman et al, 2001), inducible nitric-oxide synthase, and cyclooxygenase-2 (Lee et al, 2003). Most of these studies focused on the effects of tannins on immune cells with special regard to mononuclear cells and macrophages, and little is known regarding the possible effects of tannins in epithelial cells.…”

mentioning

confidence: 99%

Gallotannin Inhibits the Expression of Chemokines and Inflammatory Cytokines in A549 Cells

Erdélyi¹,

Kiss²,

Bakondi³

et al. 2005

Mol Pharmacol

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Tannins are plant-derived water-soluble polyphenols with wideranging biological activities. The mechanisms underlying the anti-inflammatory effect of tannins are not fully understood and may be the result of inhibition of poly(ADP-ribose) (PAR) glycohydrolase (PARG), the main catabolic enzyme of PAR metabolism. Therefore, we set out to investigate the mechanism of the anti-inflammatory effect of gallotannin (GT) in A549 cells with special regard to the role of poly(ADP-ribosyl)ation. Using an inflammation-focused low-density array and reverse transcription-polymerase chain reaction, we found that GT suppressed the expression of most cytokines and chemokines in cytokine-stimulated A549 cells, whereas the PARP inhibitor PJ-34 only inhibited few transcripts. Activation of the transcription factors, nuclear factor B (NF-B) and activator protein 1 (AP-1), was blocked by GT, whereas PJ-34 only suppressed NF-B activation but not AP-1 activation. GT also inhibited IB phosphorylation and nuclear translocation of NF-B, but PJ-34 had no effect on these upstream events. In the AP-1 pathway, GT treatment, even in the absence of cytokines, caused maximal phosphorylation of c-Jun N-terminal kinase and c-Jun. GT also caused a low-level phosphorylation of p38, extracellular signal-regulated kinases 1 and 2, activating transcription factor2, and cAMP-response element-binding protein but inhibited cytokine-induced phosphorylation of these kinases and transcription factors. GT inhibited protein phosphatases 1 and 2A, which may explain the increased phosphorylation of mitogenactivated protein kinase and their substrates. GT exerted potent antioxidant effect but failed to cause PAR accumulation. In summary, the potent inhibitory effects of GT on the transcription of cytokine and chemokine genes are probably not related to PARG inhibition. Inhibition of AP-1 activation and upstream signaling events may be responsible for the effects of GT.Tannins are water-soluble polyphenols that are widely distributed in the plant kingdom, including food grains and fruits. So far, more than a thousand different tannins have been characterized and ordered into four major groups: 1) gallotannins (GT), 2) ellagitannins, 3) complex, and 4) condensed tannins, with gallotannins and ellagitannins considered the most widespread types. The common structural elements of all tannins include one or more polyol units (mostly D-glucose) and one or more polyphenols (gallic acid, 3,4,5-trihydroxyl benzoic acid).The simplest hydrolyzable tannin, gallotannin, is a mixture of polygalloyl esthers of glucose. Gallotannin and other tannins have been shown to exert various biological effects ranging from anti-inflammatory to anticancer and antiviral effects (Fong et al., 1972;Mota et al., 1985;Uchiumi et al., 1996;Van Molle et al., 2000;Feldman et al., 2001). The mechanisms underlying the anti-inflammatory effect of tannins include the scavenging of radicals (antioxidant effect) (Hagerman et al., 1999) and inhibition of the expression of

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“…This includes the genus Rhus, Schinus, Galla, Paeoniae Radix (the root of Paeonia lactiflora Pallas), Moutan cortex (the root cortex of Paeonia suffruicos), Macaranga tanariu, Quercus pedunculata, peony, and green alga Spirogyra varians. 5GG has been found to have various biological activities; it inhibits lipopolysaccharide-stimulated tumor necrosis factor-␣ secretion (22), gastric H ϩ ,K ϩ -ATPase (23), NADH dehydrogenase I/II (24 -27), xanthine oxidase (28), and ␣-glucosidase (29). 5GG also exhibits an endothelium-dependent vasodilator effect on isolated rat aorta (30) and manifests an anticonvulsant action (31).…”

mentioning

confidence: 99%

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

Chen

Lin

2004

Journal of Biological Chemistry

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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. Pentagalloylglucose also induces apoptosis in human leukemic cells. However, the mechanisms by which pentagalloylglucose induces these effects is unclear. 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 chymotrypsinlike activity of the 26 S proteasome in intact Jurkat T cells. 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. This was shown by cycloheximide treatment and in vivo pulsechase labeling experiments, and this effect correlated with the arrest of proliferation of Jurkat T cells at G 1 . Inhibition of the proteasome by pentagalloylglucose and by the proteasome inhibitor MG132 caused accumulation of ubiquitin-tagged proteins in Jurkat T cells. The addition of pentagalloylglucose to Jurkat T cells enhanced the stability of the proteasome substrate Bax and increased cytochrome c release and apoptosis. Our findings suggest a mechanism for the effect of pentagalloylglucose on the cell cycle in human leukemic cells: that pentagalloylglucose down-regulates proteasomemediated pathways because it is a proteasome inhibitor.In eukaryotic cells, there are two distinct proteolytic mechanisms essential for regulating levels of cellular proteins. One is lysosomal mediated degradation, which is involved in the breakdown of intracellular proteins under conditions of cellular stress, membrane-associated proteins, and proteins that have entered the cell by endocytosis. The ubiquitin-proteasome pathway is the other mechanism responsible for the turnover of intracellular proteins. This second system works by marking specific substrates with ubiquitins and degrading the marked proteins by the 26 S proteasome in an ATP-dependent manner.

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In vitro and In vivo inhibition of LPS-stimulated tumor necrosis factor-α secretion by the gallotannin β- d -pentagalloylglucose

Cited by 63 publications

References 11 publications

Gallotannin inhibits NFĸB signaling and growth of human colon cancer xenografts

Gallotannin inhibits NFĸB signaling and growth of human colon cancer xenografts

Gallotannin Inhibits the Expression of Chemokines and Inflammatory Cytokines in A549 Cells

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

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