Epigallocatechin Gallate Ameliorates the Effects of Prenatal Alcohol Exposure in a Fetal Alcohol Spectrum Disorder-Like Mouse Model

Almeida-Toledano, Laura; Andreu-Férnández, Vicente; Aras-López, Rosa; Garcı́a-Algar, Óscar; Martínez, Leopoldo; Gómez-Roig, María Dolores

doi:10.3390/ijms22020715

Cited by 26 publications

(19 citation statements)

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“…Research in murine models showed increases of glutathione and superoxide dismutase levels and mitigation of lipid peroxide and nitrite levels with EGCG treatment at 50 or 100 mg/kg in rat neonates [ 80 ], as well as reduction of hydrogen peroxide (H 2 O 2 ) and malondialdehyde (MDA) production in pregnant mice treated with 400 mg/kg EGCG on gestational days (GD) 7–8 [ 79 ]. Conversely, prenatal alcohol exposure (PAE) and EGCG treatment at 30 mg/kg showed EGCG-related reduction of Nfr2 [ 81 ], probably because EGCG mainly exerts its antioxidant action through other molecular pathways such as induction of phase II detoxifying enzymes and scavenging of ROS.…”

Section: Resultsmentioning

confidence: 99%

“…Regarding fetal growth, EGCG regulates placental angiogenesis disorders and fetal growth restriction produced by PAE by maintaining adequate placental vascularization [ 79 , 81 ], as evidenced by the compensatory effect on the expression of vascular endothelial growth factor-A (VEGF-A) and vascular endothelial growth factor receptor 1 (VEGF-R1) in a mouse model of continuous ethanol exposure [ 81 ].…”

Section: Resultsmentioning

confidence: 99%

“…Moreover, outcomes from a study in a mice model of continued PAE determined that a daily dose of 30 mg/kg of EGCG could help prevent losses of mature neurons and maturation delay produced by ethanol, as indicated by changes in neuronal nuclei (NeuN) and doublecortin (DCX) expression, respectively. Similarly, EGCG up-regulates glial fibrillary acidic protein (GFAP) and brain-derived neurotrophic factor (BDNF) by compensating for early astrocyte differentiation and disturbances in neuronal plasticity generated by maternal drinking [ 81 ].…”

Section: Resultsmentioning

confidence: 99%

“…EGCG´s antioxidant properties are key for early interventions aiming to prevent secondary FASD disabilities, since one of the main pathophysiological mechanisms of alcohol-related disorders is oxidative stress. EGCG modulates antioxidant defense and oxidative stress balance in FASD-like rodent models [ 79 , 80 , 81 ], resulting in the reduction of neuronal loss and recovery of maturation delay, and prevents early astrocyte differentiation and disturbances in neuronal plasticity produced by maternal drinking [ 81 ]. Moreover, EGCG prevents neuronal apoptosis and ameliorates inflammatory response secondary to PAE [ 80 ], and regulates the expression of genes and proteins involved in brain development and neural differentiation [ 79 ] associated with improvements in memory and learning abilities [ 80 ].…”

Section: Discussionmentioning

confidence: 99%

“…Four preclinical studies on potential EGCG therapy were found in the search (summarized in Table 2), although none involved humans. EGCG reduces oxidative-nitrosative stress and enhances antioxidant defense [79][80][81]. Research in murine models showed increases of glutathione and superoxide dismutase levels and mitigation of lipid peroxide and nitrite levels with EGCG treatment at 50 or 100 mg/kg in rat neonates [80], as well as reduction of hydrogen peroxide (H 2 O 2 ) and malondialdehyde (MDA) production in pregnant mice treated with 400 mg/kg EGCG on gestational days (GD) 7-8 [79].…”

Section: Catechins In Fetal Alcohol Spectrum Disorders (Fasd)mentioning

confidence: 99%

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Therapeutic Effects of Catechins in Less Common Neurological and Neurodegenerative Disorders

et al. 2021

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In recent years, neurological and neurodegenerative disorders research has focused on altered molecular mechanisms in search of potential pharmacological targets, e.g., imbalances in mechanisms of response to oxidative stress, inflammation, apoptosis, autophagy, proliferation, differentiation, migration, and neuronal plasticity, which occur in less common neurological and neurodegenerative pathologies (Huntington disease, multiple sclerosis, fetal alcohol spectrum disorders, and Down syndrome). Here, we assess the effects of different catechins (particularly of epigalocatechin-3-gallate, EGCG) on these disorders, as well as their use in attenuating age-related cognitive decline in healthy individuals. Antioxidant and free radical scavenging properties of EGCG -due to their phenolic hydroxyl groups-, as well as its immunomodulatory, neuritogenic, and autophagic characteristics, makes this catechin a promising tool against neuroinflammation and microglia activation, common in these pathologies. Although EGCG promotes the inhibition of protein aggregation in experimental Huntington disease studies and improves the clinical severity in multiple sclerosis in animal models, its efficacy in humans remains controversial. EGCG may normalize DYRK1A (involved in neural plasticity) overproduction in Down syndrome, improving behavioral and neural phenotypes. In neurological pathologies caused by environmental agents, such as FASD, EGCG enhances antioxidant defense and regulates placental angiogenesis and neurodevelopmental processes. As demonstrated in animal models, catechins attenuate age-related cognitive decline, which results in improvements in long-term outcomes and working memory, reduction of hippocampal neuroinflammation, and enhancement of neuronal plasticity; however, further studies are needed. Catechins are valuable compounds for treating and preventing certain neurodegenerative and neurological diseases of genetic and environmental origin. However, the use of different doses of green tea extracts and EGCG makes it difficult to reach consistent conclusions for different populations.

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Section: Resultsmentioning

confidence: 99%