Role of a novel (−)-epigallocatechin-3-gallate delivery system on the prevention against oxidative stress damage in vitro and in vivo model of Parkinson's disease

Sánchez-Giraldo, Vanesa; Monsalve, Yuliana; Palacio, J.; Mendivil-Perez, Miguel; Sierra, Ligia; Vélez-Pardo, Carlos; López, Betty L.; Jiménez-Del-Río, Marlene

doi:10.1016/j.jddst.2019.101466

Cited by 14 publications

(1 citation statement)

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“…A key question then arises: can EGCG be translated to the clinic in FAD PSEN1 E280A patients [ 60 ]? Our present results and previous experimental approaches with EGCG loaded in nanoparticles (e.g., [ 61 , 62 , 63 ]) encourage its use in the treatment of FAD patients. Although the EGCG dose levels and administration route remain to be established, the EGCG nonetheless might be a promising therapeutic candidate for FAD.…”

Section: Discussionsupporting

confidence: 78%

(−)-Epigallocatechin-3-Gallate Diminishes Intra-and Extracellular Amyloid-Induced Cytotoxic Effects on Cholinergic-like Neurons from Familial Alzheimer’s Disease PSEN1 E280A

et al. 2021

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Alzheimer’s disease (AD) is a complex neurodegenerative disease characterized by functional disruption, death of cholinergic neurons (ChNs) because of intracellular and extracellular Aβ aggregates, and hyperphosphorylation of protein TAU (p-TAU). To date, there are no efficient therapies against AD. Therefore, new therapies for its treatment are in need. The goal of this investigation was to evaluate the effect of the polyphenol epigallocatechin-3-gallate (EGCG) on cholinergic-like neurons (ChLNs) bearing the mutation E280A in PRESENILIN 1 (PSEN1 E280A). To this aim, wild-type (WT) and PSEN1 E280A ChLNs were exposed to EGCG (5–50 μM) for 4 days. Untreated or treated neurons were assessed for biochemical and functional analysis. We found that EGCG (50 μM) significantly inhibited the aggregation of (i)sAPPβf, blocked p-TAU, increased ∆Ψm, decreased oxidation of DJ-1 at residue Cys106-SH, and inhibited the activation of transcription factor c-JUN and P53, PUMA, and CASPASE-3 in mutant ChLNs compared to WT. Although EGCG did not reduce (e)Aβ42, the polyphenol reversed Ca2+ influx dysregulation as a response to acetylcholine (ACh) stimuli in PSEN1 E280A ChLNs, inhibited the activation of transcription factor NF-κB, and reduced the secretion of pro-inflammatory IL-6 in wild-type astrocyte-like cells (ALCs) when exposed to mutant ChLNs culture supernatant. Taken together, our findings suggest that the EGCG might be a promising therapeutic approach for the treatment of FAD.

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