Epigallocatechin gallate and mitochondria—A story of life and death

Oliveira, Marcos Roberto de; Nabavi, Seyed Fazel; Daglia, Maria; Rastrelli, Luca

doi:10.1016/j.phrs.2015.12.027

Cited by 130 publications

(75 citation statements)

References 156 publications

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“…Such modifications also include increase in the levels of porin and mitochondrial respiratory proteins, and in mtDNA content. Therefore, epigallocatechin gallate is able to modulate systemic energy use by inducing mitochondrial changes[67]. On the other hand, this bioactive molecule has been reported to induce fatty acid β-oxidation through an increase in mRNA levels of CPT-1 and UCP2[68].…”

Section: Polyphenolsmentioning

confidence: 99%

Antioxidant dietary approach in treatment of fatty liver: New insights and updates

Ferramosca

Giacomo

Zara

2017

WJG

138

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Non-alcoholic fatty liver disease (NAFLD) is a common clinicopathological condition, encompassing a range of conditions caused by lipid deposition within liver cells. To date, no approved drugs are available for the treatment of NAFLD, despite the fact that it represents a serious and growing clinical problem in the Western world. Identification of the molecular mechanisms leading to NAFLD-related fat accumulation, mitochondrial dysfunction and oxidative balance impairment facilitates the development of specific interventions aimed at preventing the progression of hepatic steatosis. In this review, we focus our attention on the role of dysfunctions in mitochondrial bioenergetics in the pathogenesis of fatty liver. Major data from the literature about the mitochondrial targeting of some antioxidant molecules as a potential treatment for hepatic steatosis are described and critically analysed. There is ample evidence of the positive effects of several classes of antioxidants, such as polyphenols (i.e., resveratrol, quercetin, coumestrol, anthocyanins, epigallocatechin gallate and curcumin), carotenoids (i.e., lycopene, astaxanthin and fucoxanthin) and glucosinolates (i.e., glucoraphanin, sulforaphane, sinigrin and allyl-isothiocyanate), on the reversion of fatty liver. Although the mechanism of action is not yet fully elucidated, in some cases an indirect interaction with mitochondrial metabolism is expected. We believe that such knowledge will eventually translate into the development of novel therapeutic approaches for fatty liver.

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Section: Polyphenolsmentioning

confidence: 99%

Antioxidant dietary approach in treatment of fatty liver: New insights and updates

Ferramosca

Giacomo

Zara

2017

WJG

138

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“…The potent antioxidant and anti-inflammatory activities of EGCG are also beneficial to the modulation of mitochondrial functions, impacting mitochondrial bioenergetic control, cell cycle, and mitochondria-related apoptosis [30]. …”

Section: Mechanism Of Tea Catechins In Suppressing Breast Cancermentioning

confidence: 99%

“…The important nodes in this pathway are used as key therapeutic targets for cancer treatments. EGCG was confirmed to be an ATP-competitive inhibitor of both PI3K and mTOR in breast cancer cells MDA-MB-231, with Ki values ranging 380 nM to 320 nM, respectively [30]. Molecular docking studies showed that EGCG binds well to the PI3K kinase domain active site, showing ATP-competitive activity [31].…”

Section: Mechanism Of Tea Catechins In Suppressing Breast Cancermentioning

confidence: 99%

Suppressive Effects of Tea Catechins on Breast Cancer

Xiang

Wang²,

et al. 2016

Nutrients

101

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Tea leaf (Camellia sinensis) is rich in catechins, which endow tea with various health benefits. There are more than ten catechin compounds in tea, among which epigallocatechingallate (EGCG) is the most abundant. Epidemiological studies on the association between tea consumption and the risk of breast cancer were summarized, and the inhibitory effects of tea catechins on breast cancer, with EGCG as a representative compound, were reviewed in the present paper. The controversial results regarding the role of tea in breast cancer and areas for further study were discussed.

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“…Epigallocatechin-3-gallate (EGCG), a polyphenol in green tea, is an important dietary antioxidant molecule with anti-inflammatory and cytoprotective abilities, protecting cells from mitochondria-related apoptosis [13][14][15]. Neuroprotective functions of EGCG are accomplished by radical scavenging, metal chelation and inducing range of cellular mechanisms including activation and inhibition of signalling pathways (PKC, MAPK and PI3K/Akt) [16].…”

Section: Introductionmentioning

confidence: 99%

Epigallocatechin gallate protects BEAS-2B cells from lipopolysaccharide-induced apoptosis through upregulation of gastrin-releasing peptide

et al. 2017

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Gastrin-releasing peptide (GRP) plays a major role in the development and maintenance of lung epithelial cells by promoting cell division, whereas its suppression causes growth arrest and apoptosis. The present study shows that human bronchial epithelial BEAS-2B cells challenged with lipopolysaccharide (LPS), an endotoxin from gram-negative bacteria, downregulated GRP expression and induced apoptosis via upregulation of p53 and active caspase-3, signifying the importance of GRP in lung epithelial cell survival. However, in the presence of epigallocatechin-3-gallate (EGCG), a polyphenol in green tea, BEAS-2B cells resisted LPS-induced apoptosis and restored the expression of GRP and its downstream effectors such as epidermal growth factor receptor and NF-κB, as analysed by immunoblotting and qPCR. Based on our findings, we objectify that cytoprotective functions of EGCG, via upregulation of GRP in cells challenged with LPS, are novel and can be further explored in a therapeutic point of view for diseases such as septic shock.

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Epigallocatechin gallate and mitochondria—A story of life and death

Cited by 130 publications

References 156 publications

Antioxidant dietary approach in treatment of fatty liver: New insights and updates

Antioxidant dietary approach in treatment of fatty liver: New insights and updates

Suppressive Effects of Tea Catechins on Breast Cancer

Epigallocatechin gallate protects BEAS-2B cells from lipopolysaccharide-induced apoptosis through upregulation of gastrin-releasing peptide

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