Effects of green tea epigallocatechin-3-gallate on the proteolipid protein and oligodendrocyte transcription factor 1 messenger RNA gene expression in a mouse model of multiple sclerosis

Semnani, Mohammad-Reza; Mashayekhi, Farhad; Azarnia, Mahnaz; Salehi, Zivar

doi:10.5114/fn.2017.70484

Cited by 16 publications

(14 citation statements)

References 35 publications

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“…In mice, EGCG has been shown to protect against ischemia reperfusion injury in a NRF2dependent manner (Han et al, 2014) and has also been shown to inhibit NFkB activity, reduce Ab fibrilization, and improve memory in Ab exposed animals (Lee et al, 2009b). Neuroprotective effects of EGCG have also been demonstrated in vitro and in vivo in models of PD, MS, and TBI accompanied by increased NRF2 activity and enhanced antioxidant activity and reduced inflammatory responses (Ma et al, 2010;Itoh et al, 2013;Wu, 2016;Semnani et al, 2017;Xu et al, 2018).…”

Section: Botanically Derived Nrf2 Activatorsmentioning

confidence: 99%

NRF2 as a Therapeutic Target in Neurodegenerative Diseases

2020

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Increased reactive oxygen species production and oxidative stress have been implicated in the pathogenesis of numerous neurodegenerative conditions including among others Alzheimer's disease, Parkinson's disease, Huntington's disease, Friedrich's ataxia, multiple sclerosis, and stroke. The endogenous antioxidant response pathway protects cells from oxidative stress by increasing the expression of cytoprotective enzymes and is regulated by the transcription factor nuclear factor erythroid 2-related factor 2 (NRF2). In addition to regulating the expression of antioxidant genes, NRF2 has also been shown to exert anti-inflammatory effects and modulate both mitochondrial function and biogenesis. This is because mitochondrial dysfunction and neuroinflammation are features of many neurodegenerative diseases as well NRF2 has emerged as a promising therapeutic target. Here, we review evidence for a beneficial role of NRF2 in neurodegenerative conditions and the potential of specific NRF2 activators as therapeutic agents.

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Section: Botanically Derived Nrf2 Activatorsmentioning

confidence: 99%

NRF2 as a Therapeutic Target in Neurodegenerative Diseases

2020

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“…The results showed that 50 mg/kg of body weight per day EGCG for four weeks increases myelin proteolipid protein (PLP) and oligodendrocyte transcription factor 1 (Olig1) expression in the cerebral cortex of cuprizone mouse model (C57BL/6 mice). PLP plays an important role in the formation or maintenance of the multilamellar structure of myelin, and Olig1 is a key regulatory factor of myelin specific gene expression and the program of myelinogenesis [102]. The combined application of EGCG and GA synergistically reduced cell death and promoted the axonal outgrowth of primary neurons.…”

Section: Antioxidant Compounds As Complementary Therapy In Msmentioning

confidence: 99%

A Review of Various Antioxidant Compounds and their Potential Utility as Complementary Therapy in Multiple Sclerosis

et al. 2019

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Multiple sclerosis (MS) is a complex disease of the central nervous system (CNS). The etiology of this multifactorial disease has not been clearly defined. Conventional medical treatment of MS has progressed, but is still based on symptomatic treatment. One of the key factors in the pathogenesis of MS is oxidative stress, enhancing inflammation and neurodegeneration. In MS, both reactive oxygen and nitrogen species are formed in the CNS mainly by activated macrophages and microglia structures, which can lead to demyelination and axon disruption. The course of MS is associated with the secretion of many inflammatory and oxidative stress mediators, including cytokines (IL-1b, IL-6, IL-17, TNF-α, INF-γ) and chemokines (MIP-1a, MCP-1, IP10). The early stage of MS (RRMS) lasts about 10 years, and is dominated by inflammatory processes, whereas the chronic stage is associated with neurodegenerative axon and neuron loss. Since oxidative damage has been known to be involved in inflammatory and autoimmune-mediated processes, antioxidant therapy could contribute to the reduction or even prevention of the progression of MS. Further research is needed in order to establish new aims for novel treatment and provide possible benefits to MS patients. The present review examines the roles of oxidative stress and non-pharmacological anti-oxidative therapies in MS.

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“…Other studies used a cuprizone-induced MS mice model to test the effects of EGCG. EGCG significantly increased the proteolipid protein and oligodendrocyte transcription factor 1 in the cerebral cortex, which is related to the remyelination process [ 62 , 63 ]. Both animal models showed that EGCG treatment improves clinical symptoms or molecular mechanisms of the affected mice.…”

Section: Resultsmentioning

confidence: 99%

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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Effects of green tea epigallocatechin-3-gallate on the proteolipid protein and oligodendrocyte transcription factor 1 messenger RNA gene expression in a mouse model of multiple sclerosis

Cited by 16 publications

References 35 publications

NRF2 as a Therapeutic Target in Neurodegenerative Diseases

NRF2 as a Therapeutic Target in Neurodegenerative Diseases

A Review of Various Antioxidant Compounds and their Potential Utility as Complementary Therapy in Multiple Sclerosis

Therapeutic Effects of Catechins in Less Common Neurological and Neurodegenerative Disorders

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