Epigallocatechin-3-gallate augments antioxidant activities and inhibits inflammation during bleomycin-induced experimental pulmonary fibrosis through Nrf2–Keap1 signaling

Narayanan, Sriram; Srinivasan, Kannan; Sudhandiran, Ganapasam

doi:10.1016/j.pupt.2008.12.010

Cited by 161 publications

(114 citation statements)

References 64 publications

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“…In the present study, we observed that cells exposed to TNF-α attenuated the Nrf2 DNA-binding activity, which, however, was specially reversed by pretreatment with EGCG. Western blot analysis data also showed that EGCG decreased cytosolic protein levels and enhanced cellular nuclear Nrf2 protein levels in THP-1 macrophage cell lines, which was in agreement with the results of studies in rats with pulmonary fibrosis and rats with lupus nephritis (28,29). Thus, it is clear that EGCG induces the cytosolic Nrf2 translocation to the nucleus and activates the transcription of genes containing an ARE element in their promoter regions resulting in inhibition of TNF-α-induced NF-κB activity.…”

Section: Discussionsupporting

confidence: 89%

“…To further examine the involvement of important cellular components in cell fate, we focused first on Nrf2 based on the facts that EGCG activates it (18,28,29). EGCG has been reported to have anti-inflammatory effects by increasing nuclear Nrf2 activities and inhibiting nuclear NF-κB-mediated inflammatory responses in vivo (29).…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have indicated the involvement of Nrf2-Keap1 signaling in EGCG enhanced antioxidant activities with subsequent restraints NF-κB activation (18,28,29). The main function of Nrf2 is to activate the antioxidant response and induce transcription of a wide array of genes that is able to combat the harmful effects of oxidative stress and inflammation.…”

Section: Egcg Prevents Tnf-α-induced Nf-κb Activation and Upregulatesmentioning

confidence: 99%

“…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). Nrf2 is indispensable to cellular defense against many chemical insults of endogenous and exogenous origin, which plays a major role in the etiopathogenesis of many cancers and inflammation-related diseases (30).…”

Section: Introductionmentioning

confidence: 99%

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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: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 99%

Section: Egcg Prevents Tnf-α-induced Nf-κb Activation and Upregulatesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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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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“…Interestingly, EGCG was shown to effectively induce Nrf2 and, as a consequence, enhance antioxidant activities of Phase II enzymes, and to reduce inflammation. 49,50 …”

Section: Pulmonary Fibrosismentioning

confidence: 99%

Green tea polyphenol epigallocatechin-3-gallate (EGCG) as adjuvant in cancer therapy

et al. 2013

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s u m m a r yBackground & aims: Green tea catechins, especially epigallocatechin-3-gallate (EGCG), have been associated with cancer prevention and treatment. This has resulted in an increased number of studies evaluating the effects derived from the use of this compound in combination with chemo/radiotherapy. This review aims at compiling latest literature on this subject. Methods: Keywords including EGCG, cancer, chemotherapy, radiotherapy and side effects, were searched using PubMed and ScienceDirect databases to identify, analyze, and summarize the research literature on this topic. Most of the studies on this subject up to date are preclinical. Relevance of the findings, impact factor, and date of publication were critical parameters for the studies to be included in the review. Results: Additive and synergistic effects of EGCG when combined with conventional cancer therapies have been proposed, and its anti-inflammatory and antioxidant activities have been related to amelioration of cancer therapy side effects. However, antagonistic interactions with certain anticancer drugs might limit its clinical use. Conclusions: The use of EGCG could enhance the effect of conventional cancer therapies through additive or synergistic effects as well as through amelioration of deleterious side effects. Further research, especially at the clinical level, is needed to ascertain the potential role of EGCG as adjuvant in cancer therapy.

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Nutraceuticals and Antioxidant Function

Young¹,

Tsao²,

Mine³

2011

Functional Foods, Nutraceuticals, and Degenerative Disease Prevention

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Epigallocatechin-3-gallate augments antioxidant activities and inhibits inflammation during bleomycin-induced experimental pulmonary fibrosis through Nrf2–Keap1 signaling

Cited by 161 publications

References 64 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

Green tea polyphenol epigallocatechin-3-gallate (EGCG) as adjuvant in cancer therapy

Nutraceuticals and Antioxidant Function

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