The impact of blue light in monolayers representing tumorigenic and nontumorigenic cell membranes containing epigallocatechin-3-gallate

Pires, Filipa; Magalhães-Mota, Gonçalo; Geraldo, Vananélia P.N.; Ribeiro, Paulo A.; Oliveira, Osvaldo N.; Raposo, Maria

doi:10.1016/j.colsurfb.2020.111129

Cited by 14 publications

(7 citation statements)

References 45 publications

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“…Moreover, the presence of EGCG in the binding site suggested by our simulations would hamper the rotation of the A-domain which is critical for the E1P to E2P transition in P-type ATPases (Figure 6C) [45,46]. On the other hand, the binding of EGCG to the N-domain near the ATP binding site was also evaluated since EGCG would be near the phosphorylation site and EGCG interacts with phosphate groups [47,48]. However, EGCG binding to this site would not explain why EGCG blocks the PMCA reaction cycle in E1P, making it less likely of being responsible for PMCA Ca 2þ -ATPase activity inhibition at low EGCG concentrations.…”

Section: Docking Simulationsmentioning

confidence: 99%

Epigallocatechin 3-gallate inhibits the plasma membrane Ca2+-ATPase: effects on calcium homeostasis

Rinaldi

Ontiveros

Saffioti

et al. 2021

Heliyon

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Section: Docking Simulationsmentioning

confidence: 99%

Epigallocatechin 3-gallate inhibits the plasma membrane Ca2+-ATPase: effects on calcium homeostasis

Rinaldi

Ontiveros

Saffioti

et al. 2021

Heliyon

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“…Accumulating evidence has suggested a number of sources and mechanisms for oxidative stress in PD, which include nicotinamide adenine dinucleotide phosphate oxidase (NOX) activation, mitochondrial dysfunction, the catabolism of dopamine by auto-oxidation, iron (Fe 2+ ) accumulation ( Wang et al, 2021 ). Oxidative stress causes injury to macromolecular components (i.e., DNA, proteins, and lipids) ( Pires et al, 2019a ; 2019b ; 2019c ; 2019d , 2020 ), resulting in cellular dysfunction and, eventually, dopaminergic neuron death ( Wang et al, 2021 ). Given the important role of oxidative stress in PD, antioxidant supplements could be a reasonable therapeutic approach to halting PD progression ( Chang and Chen, 2020 ), as it could mitigate oxidative stress-dependent neuronal injury ( Buendia et al, 2016 ).…”

Section: Introductionmentioning

confidence: 99%

Epigallocatechin-3-gallate: A phytochemical as a promising drug candidate for the treatment of Parkinson’s disease

Wang

et al. 2022

Front. Pharmacol.

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Epigallocatechin 3-gallate (EGCG), an abundant polyphenolic component derived from green tea extract, possesses versatile bioactivities that can combat many diseases. During the last decade, EGCG was shown to be effective in experimental models of Parkinson’s disease (PD). Several experimental studies have suggested that it has pleiotropic neuroprotective effects, which has enhanced the appeal of EGCG as a therapeutic strategy in PD. In this review, we compiled recent updates and knowledge of the molecular mechanisms underlying the neuroprotective effects of EGCG in PD. We focused on the effects of EGCG on apoptosis, oxidative stress, inflammation, ferroptosis, modulation of dopamine production, and the aggregation of α-synuclein. The review highlights the pharmacological features of EGCG and its therapeutic implications in PD. Taken together, the accumulated data indicate that EGCG is a promising neuroprotective compound for the treatment of PD.

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“…It exhibits potent neuroprotective, hypoglycemic, antioxidant, antibacterial, antiviral, anti-tumor ( 7 , 8 ) and radioprotective effects in various tissues ( 9 ). Additionally, EGCG protects phospholipid molecules against the oxidative damage induced by ultraviolet radiation and blue light irradiation ( 10 – 12 ). Novel nanofiber formulations containing EGCG have the ability to scavenge the toxic reactive oxygen species (ROS) generated by exposure to either H 2 O 2 or ultraviolet radiation and significantly accelerates the wound-healing process ( 13 ).…”

Section: Introductionmentioning

confidence: 99%

(-)-Epigallocatechin-3-Gallate (EGCG) Modulates the Composition of the Gut Microbiota to Protect Against Radiation-Induced Intestinal Injury in Mice

Cai

Xie

et al. 2022

Front. Oncol.

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The high radiosensitivity of the intestinal epithelium limits the outcomes of radiotherapy against abdominal malignancies, which results in poor prognosis. Currently, no effective prophylactic or therapeutic strategy is available to mitigate radiation toxicity in the intestine. Our previous study revealed that the green tea polyphenol (-)-epigallocatechin-3-gallate (EGCG) attenuates radiation-induced intestinal injury (RIII). The aim of the present study was to determine the effect of EGCG on the intestinal flora of irradiated mice. EGCG administration reduced radiation-induced intestinal mucosal injury, and significantly increased the number of Lgr5+ intestinal stem cells (ISCs) and Ki67+ crypt cells. In addition, EGCG reversed radiation-induced gut dysbiosis, restored the Firmicutes/Bacteroidetes ratio, and increased the abundance of beneficial bacteria. Our findings provide novel insight into EGCG-mediated remission of RIII, revealing that EGCG could be a potential modulator of gut microbiota to prevent and treat RIII.

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The impact of blue light in monolayers representing tumorigenic and nontumorigenic cell membranes containing epigallocatechin-3-gallate

Cited by 14 publications

References 45 publications

Epigallocatechin 3-gallate inhibits the plasma membrane Ca2+-ATPase: effects on calcium homeostasis

Epigallocatechin 3-gallate inhibits the plasma membrane Ca2+-ATPase: effects on calcium homeostasis

Epigallocatechin-3-gallate: A phytochemical as a promising drug candidate for the treatment of Parkinson’s disease

(-)-Epigallocatechin-3-Gallate (EGCG) Modulates the Composition of the Gut Microbiota to Protect Against Radiation-Induced Intestinal Injury in Mice

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