Epigallocatechin-gallate stimulates NF-E2-related factor and heme oxygenase-1 via caveolin-1 displacement

Zheng, Yuanyuan; Morris, Andrew J.; Sunkara, Manjula; Layne, Joseph D.; Toborek, Michał; Hennig, Bernhard

doi:10.1016/j.jnutbio.2010.12.002

Cited by 59 publications

(43 citation statements)

References 36 publications

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“…It is reported that a 67-kDa laminin receptor (67LR), as the cell surface EGCG receptor, may be involved in mediating these actions of EGCG (22)(23)(24)(25). Moreover, EGCG is also believed to exert an Epigallocatechin-3-gallate prevents TNF-α-induced NF-κB activation thereby upregulating ABCA1 via the Nrf2/Keap1 pathway in macrophage foam cells anti-atherosclerotic effect via anti-inflammatory and metabolic regulation activities (26,27). It has also been proposed that EGCG could restrain inflammatory cytokines, such as TNF-α and IL-1β, through blocking NF-κB pathway, and nuclear factor E2-related factor 2 (Nrf2) might be involved in this process (18,28,29).…”

Section: Introductionmentioning

confidence: 99%

Epigallocatechin-3-gallate prevents TNF-α-induced NF-κB activation thereby upregulating ABCA1 via the Nrf2/Keap1 pathway in macrophage foam cells

et al. 2012

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Abstract. The ATP-binding membrane cassette transporter A1 (ABCA1) plays a protective role in the development of atherosclerosis for the reverse cholesterol transport process. Epigallocatechin-3-gallate (EGCG), which exists abundantly in green tea, exerts an anti-atherosclerotic effect via antiinflammatory and metabolic regulation activities. Many genes and proteins related to lipid metabolism are involved in the lowering cholesterol effects of EGCG. However, effects of EGCG on ABCA1 have rarely been described. In the study presented here, we found that exposure of macrophage foam cells to TNF-α results in a downregulation of ABCA1 and a decrease in cholesterol efflux to apoA1, which is attenuated by pretreatment with EGCG. Moreover, rather than activating the Liver X receptor (LXR) pathway, inhibition of the TNF-α-induced nuclear factor-κB (NF-κB) activity is detected with EGCG treatment in cells. In order to inhibit the NF-κB activity, EGCG can promote the dissociation of the nuclear factor E2-related factor 2 (Nrf2)-Kelch-like ECH-associated protein 1 (Keap1) complex; when the released Nrf2 translocates to the nucleus and activates the transcription of genes containing an ARE element inhibition of NF-κB occurs and Keap1 is separated from the complex to directly interact with IKKβ and thus represses NF-κB function. These results provide novel insight into the anti-inflammatory effects of EGCG, as well as the identification of a novel potential therapeutic role for the prevention of atherosclerosis.

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Section: Introductionmentioning

confidence: 99%

Epigallocatechin-3-gallate prevents TNF-α-induced NF-κB activation thereby upregulating ABCA1 via the Nrf2/Keap1 pathway in macrophage foam cells

et al. 2012

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“…M marker, B unstimulated cells, C PMA plus A23187-stimulated cells promising treatment and prevention of inflammation-related conditions. EGCG is the most abundant catechin in green tea (Zheng et al 2011). We therefore investigated the natural product-based compound EGCG as a natural product-based anti-inflammatory agent.…”

Section: Discussionmentioning

confidence: 99%

“…1) (Zheng et al 2011). EGCG has various effects such as anti-arthritic, anti-inflammatory, and anti-oxidant effects (Ahemd et al 2008;Wheeler et al 2004a;Rah et al 2005).…”

Section: Introductionmentioning

confidence: 99%

Epigallocatechin-3-O-gallate inhibits the production of thymic stromal lymphopoietin by the blockade of caspase-1/NF-κB pathway in mast cells

2011

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The cytokine thymic stromal lymphopoietin (TSLP) has been implicated in the development and progression of allergic diseases such as atopic dermatitis, asthma, and chronic obstructive pulmonary disease. However, it has not yet been clarified the effect of epigallocatechin-3-O-gallate (EGCG) on the production of TSLP. Thus, we investigated how EGCG inhibits the production of TSLP in the human mast cell line (HMC-1) cells. Enzyme-linked immunosorbent assay, reverse transcription-polymerase chain reaction, luciferase assay, and Western blot analysis were used to investigate the effects of EGCG. EGCG inhibited the production and mRNA expression of TSLP in HMC-1 cells. EGCG also inhibited the nuclear factor-κB luciferase activity induced by phorbol myristate acetate plus A23187. Furthermore, EGCG inhibited the activation of caspase-1 in HMC-1 cells. These results provide evidence that EGCG can help us to treat inflammatory and atopic diseases through the inhibition of TSLP.

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“…In another study, EGCG increased the level of HO-1 expression by Nrf-2 activation in endothelial cells, resulting in the passage of caveolin-1 from the plasma membrane to the cytosol, accumulating in the caveolae-regulating signaling pathways associated with vascular disease pathology [60]. Accordingly, EGCG may reduce endothelial inflammation and protect against atherosclerosis [61]. EGCG also showed a protective effect against oxidative stress-induced cerebral ischemia through Nrf2/ARE activation [62].…”

Section: Epigallocatechin Gallatementioning

confidence: 98%

Stress Response of Dietary Phytochemicals in a Hormetic Manner for Health and Longevity

Gezer¹

2018

Gene Expression and Regulation in Mammalian Cells - Transcription Toward the Establishment of Novel Therapeutics

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The stress responses observed in mammalian cells can be classified as heat shock response, unfolded protein response, autophagic response, deoxyribonucleic acid damage response, antioxidant response, and sirtuin response at the intracellular and molecular levels. Factors that strengthen the hemodynamic structure causing low-level molecular damage and activating one or several stress response pathways are called hormetins. Hormetins can be categorized as physical, physiological, biological, and nutritional hormetins. Nutritional hormetins provide an interesting, comprehensive research topic because of their effects on health and lifespan. Dietary phytochemicals, with their low-level stress-inducing effects, are potential nutritional hormetins. Resveratrol, curcumin, epicatechin, isothiocyanates, ferulic acid, and certain vitamin-minerals can induce a heat shock response, unfolded protein response, autophagic response, deoxyribonucleic acid damage response, antioxidant response, and sirtuin response causing the stimulation of kinases and transcription factors. Studies have shown that these phytochemicals are related to nuclear factor-erythroid 2, sirtuins, nuclear factor-kappa B, and heat shock response pathways. In this chapter, the stress response of dietary phytochemicals will be systematically examined in a hormetic manner for delay of age-related diseases, healthy aging, and longevity based on current data.

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Epigallocatechin-gallate stimulates NF-E2-related factor and heme oxygenase-1 via caveolin-1 displacement

Cited by 59 publications

References 36 publications

Epigallocatechin-3-gallate prevents TNF-α-induced NF-κB activation thereby upregulating ABCA1 via the Nrf2/Keap1 pathway in macrophage foam cells

Epigallocatechin-3-gallate prevents TNF-α-induced NF-κB activation thereby upregulating ABCA1 via the Nrf2/Keap1 pathway in macrophage foam cells

Epigallocatechin-3-O-gallate inhibits the production of thymic stromal lymphopoietin by the blockade of caspase-1/NF-κB pathway in mast cells

Stress Response of Dietary Phytochemicals in a Hormetic Manner for Health and Longevity

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