Fenton Reaction Is Primarily Involved in a Mechanism of (−)-Epigallocatechin-3-gallate to Induce Osteoclastic Cell Death

Nakagawa, Hiroshi; Wachi, Masaaki; Woo, Je‐Tae; Kato, Masanori; Kasai, Shinya; Takahashi, Fumiyuki; Lee, In-Seon; Nagai, Kazuo

doi:10.1006/bbrc.2002.6622

Cited by 152 publications

(118 citation statements)

References 43 publications

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“…1). In contrast, this same concentration range has been applied to tumor cell cultures and induced apoptotic effects (Suganuma et al, 1999;Chen et al, 2000;Jin et al, 2001;Yokoyama et al, 2001;Nakagawa et al, 2002;Nie et al, 2002). This evidence suggests that the effect of EGCG on exponentially growing keratinocytes is a selective induction of differentiation, in contrast to the apoptotic cell death initiated in tumor cells.…”

Section: Downloaded Frommentioning

confidence: 99%

Green Tea Polyphenols Induce Differentiation and Proliferation in Epidermal Keratinocytes

Hsu

Bollag²,

Lewis

et al. 2003

J Pharmacol Exp Ther

144

103

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The most abundant green tea polyphenol, epigallocatechin-3-gallate (EGCG), was found to induce differential effects between tumor cells and normal cells. Nevertheless, how normal epithelial cells respond to the polyphenol at concentrations for which tumor cells undergo apoptosis is undefined. The current study tested exponentially growing and aged primary human epidermal keratinocytes in response to EGCG or a mixture of the four major green tea polyphenols. EGCG elicited cell differentiation with associated induction of p57/KIP2 within 24 h in growing keratinocytes, measured by the expression of keratin 1, filaggrin, and transglutaminase activity. Aged keratinocytes, which exhibited low basal cellular activities after culturing in growth medium for up to 25 days, renewed DNA synthesis and activated succinate dehydrogenase up to 37-fold upon exposure to either EGCG or the polyphenols. These results suggest that tea polyphenols may be used for treatment of wounds or certain skin conditions characterized by altered cellular activities or metabolism.Green tea polyphenols (referred to as GTPPs, to include the four major polyphenols: epicatechin, epigallocatechin, epcatechin-3-gallate, and epigallocatechin-3-gallate (EGCG) have been identified to possess chemopreventive and apoptotic activity against certain cancers, whereas normal epidermal keratinocytes follow a survival pathway that has not been fully elucidated (Chen et al

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Section: Downloaded Frommentioning

confidence: 99%

Green Tea Polyphenols Induce Differentiation and Proliferation in Epidermal Keratinocytes

Hsu

Bollag²,

Lewis

et al. 2003

J Pharmacol Exp Ther

144

103

View full text Add to dashboard Cite

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“…In addition, it was shown that catechin has an inhibitory effect on bone resorption (20). Consistent with this, catechin reportedly induces apoptotic cell death of osteoclasts (32). Moreover, it was reported that catechin increases cell viability and alkaline phosphatase activity in osteoblast-like MC3T3-E1 cells and apoptosis of these cells is suppressed by catechin (21).…”

Section: Discussionmentioning

confidence: 65%

(−)-Epigallocatechin gallate attenuates the induction of HSP27 stimulated by sphingosine 1-phosphate via suppression of phosphatidylinositol 3-kinase/Akt pathway in osteoblasts

Natsume

Adachi²,

Takai³

et al. 2009

Int J Mol Med

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Abstract. We previously reported that sphingosine 1-phosphate stimulates the induction of heat shock protein 27 (HSP27) through p38 mitogen-activated protein (MAP) kinase and phosphatidylinositol 3-kinase/Akt in osteoblast-like MC3T3-E1 cells. In the present study, we investigated whether (-)-epigallocatechin gallate (EGCG), the major polyphenol found in green tea, affects the induction of HSP27 in these cells and its mechanism, since it was previously reported that catechin, including EGCG, suppresses bone resorption. EGCG significantly reduced the induction of HSP27 stimulated by sphingosine 1-phosphate in a dose-dependent manner between 10 and 30 μM. Immunofluorescence microscopy studies revealed that sphingosine 1-phosphate certainly stimulated the induction of HSP27 in the cytosol of these cells, and that EGCG clearly suppressed its induction. However, sphingosine 1-phosphate-stimulated phosphorylation of p38 MAP kinase or MAPKAP-2 was not affected by EGCG. By contrast, EGCG markedly suppressed the phosphorylations of both Akt and glycogen synthase kinase-3ß stimulated by sphingosine 1-phosphate. These results strongly suggest that EGCG suppresses the induction of HSP27 stimulated by sphingosine 1-phosphate via attenuation of, not the p38 MAP kinase pathway, but of the phosphatidylinositol 3-kinase/Akt pathway in osteoblasts.

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“…In this study, we examined the effects of an antioxidant EGCG, a catechin that reportedly eliminates ROS in vitro (17,18) and reduces oxidative stress markers such as 8-OHdG and total MDA in humans and animals. Interestingly, we found that supplementation with 0.1% EGCG reduced the gene expressions of inflammatory cytokines (TNF-a, IFN-g, IL-1b, IL-6, and IL-18), integrins (CD11b), S100 proteins (S100a6), and MCP-1 in peripheral leukocytes of GK rats.…”

Section: Discussionmentioning

confidence: 99%

“…It was reported that consumption of green tea extracts or EGCG has beneficial effects on blood glucose control in obese and type 2 diabetic humans (14), mice (15), and rats (16). It has already been shown that EGCG eliminates ROS in vitro (17,18) and reduces 8-hydroxydeoxyguanosine (OHdG), which is a product of DNA oxidation by ROS (19). It appears likely that intake of EGCG or green tea reduces proinflammatory cytokine expression in leukocytes, and that the reduction leads to decreased development of type 2 diabetes and related complications.…”

Section: Dietary Supplementation With a Low Dose Of (2)-epigallocatecmentioning

confidence: 99%

Dietary Supplementation with a Low Dose of (^|^minus;)-Epigallocatechin-3-Gallate Reduces Pro-Inflammatory Responses in Peripheral Leukocytes of Non-Obese Type 2 Diabetic GK Rats

Uchiyama

Suzuki

Mochizuki

et al. 2013

J Nutr Sci Vitaminol

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Summary (2)-Epigallocatechin-3-gallate (EGCG), which is largely found in green tea, is known to eliminate reactive oxygen species and associated inflammatory responses in vitro and in cells. However, the in vivo mechanisms underlying the effects of EGCG on the amelioration of metabolic disorders are not fully understood. In this study, we examined whether dietary supplementation with EGCG reduces inflammatory responses in peripheral leukocytes of a non-obese type 2 diabetes animal model, Goto-Kakizaki (GK) rats. GK rats at 9 wk of age were fed a control high-fat diet (46 energy % from lard and corn oil) or a high-fat diet containing 0.1%, 0.2%, or 0.5% EGCG (w/w) for 25 wk. The oxidative stress markers 8-hydroxydeoxyguanosine (OHdG) and total malondialdehyde (MDA) were reduced by supplementation with EGCG at 0.1%, but not at 0.2% or more. Significant reductions in the mRNA levels of genes related to inflammatory responses (TNF-a, IFN-g, IL-1b, IL-6, IL-18, MCP-1, CD11b, and S100a6), 8-OHdG, and total MDA were induced in peripheral leukocytes of GK rats by EGCG supplementation at 0.1%, but not at 0.2% or more, compared with rats fed the control diet. The present results suggest that supplementation with a low dose of EGCG reduces oxidative stress and the expressions of genes involved in inflammation in peripheral leukocytes of GK rats.

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Fenton Reaction Is Primarily Involved in a Mechanism of (−)-Epigallocatechin-3-gallate to Induce Osteoclastic Cell Death

Cited by 152 publications

References 43 publications

Green Tea Polyphenols Induce Differentiation and Proliferation in Epidermal Keratinocytes

Green Tea Polyphenols Induce Differentiation and Proliferation in Epidermal Keratinocytes

(−)-Epigallocatechin gallate attenuates the induction of HSP27 stimulated by sphingosine 1-phosphate via suppression of phosphatidylinositol 3-kinase/Akt pathway in osteoblasts

Dietary Supplementation with a Low Dose of (^|^minus;)-Epigallocatechin-3-Gallate Reduces Pro-Inflammatory Responses in Peripheral Leukocytes of Non-Obese Type 2 Diabetic GK Rats

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