Effects and mechanism of epigallocatechin-3-gallate on apoptosis and mTOR/AKT/GSK-3β pathway in substantia nigra neurons in Parkinson rats

Zhou, Wei; Chen, Lei; Hu, Xiqing; Cao, Shanshan; Yang, Junxiu

doi:10.1097/wnr.0000000000001149

Cited by 25 publications

(12 citation statements)

References 25 publications

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“…Ellagic acid [214] Entacapone (Comtan, ASI-6) [12,215,216] Enzastaurin [164] Epicatechin [128,160,193,194] Epigallocatechin-3-gallate [117,217,218] Etidronate (HEDPA) [219] Exifone [12] F13714 [220] F15599 [220,221] Farrerol [222] Fisetin (3,3 ,4 ,7-Tetrahydroxy flavone) [223][224][225] Fraxetin [117] Galangin [226] Gallic acid and derivatives [214,227,228] Gallocatechin [128] Garcinol [229] Genistein [117,128,230,231] Glutamine [232] Glutathione derivatives [63] Glutathione -hydroxyquinoline compound [233] Glutathione-l-DOPA compound [234] Gly-N-C-DOPA [209] GSK2795039 [108] Guanabenz [235] Hesperidin [128,236] Hinokitiol […”

Section: Compound Name(s) Referencesmentioning

confidence: 99%

Metal Chelation Therapy and Parkinson’s Disease: A Critical Review on the Thermodynamics of Complex Formation between Relevant Metal Ions and Promising or Established Drugs

Tosato

Marco

2019

Biomolecules

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The present review reports a list of approximately 800 compounds which have been used, tested or proposed for Parkinson’s disease (PD) therapy in the year range 2014–2019 (April): name(s), chemical structure and references are given. Among these compounds, approximately 250 have possible or established metal-chelating properties towards Cu(II), Cu(I), Fe(III), Fe(II), Mn(II), and Zn(II), which are considered to be involved in metal dyshomeostasis during PD. Speciation information regarding the complexes formed by these ions and the 250 compounds has been collected or, if not experimentally available, has been estimated from similar molecules. Stoichiometries and stability constants of the complexes have been reported; values of the cologarithm of the concentration of free metal ion at equilibrium (pM), and of the dissociation constant Kd (both computed at pH = 7.4 and at total metal and ligand concentrations of 10–6 and 10–5 mol/L, respectively), charge and stoichiometry of the most abundant metal–ligand complexes existing at physiological conditions, have been obtained. A rigorous definition of the reported amounts is given, the possible usefulness of this data is described, and the need to characterize the metal–ligand speciation of PD drugs is underlined.

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Section: Compound Name(s) Referencesmentioning

confidence: 99%

Metal Chelation Therapy and Parkinson’s Disease: A Critical Review on the Thermodynamics of Complex Formation between Relevant Metal Ions and Promising or Established Drugs

Tosato

Marco

2019

Biomolecules

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“…Ahmad Rather et al reported that asiatic acid inhibited aluminium chloride–induced tau pathology, oxidative stress and apoptosis via the AKT/GSK‐3β signalling pathway in Wistar rats. Zhou et al revealed that epigallocatechin‐3‐gallate reduced apoptosis in substantia nigra neurons in Parkinson's model rats through mTOR/AKT/GSK‐3β activation. Therefore, miR‐21 has an ability to regulate PI3K/AKT/GSK‐3β signalling, and activation of AKT/GSK‐3β plays a protective role in many neurological diseases.…”

Section: Discussionmentioning

confidence: 99%

“…Many studies indicate that miR‐21 can activate the PI3K/AKT signalling pathway in models of Alzheimer's disease and several malignant tumours . Other studies found that activation of the AKT/GSK‐3β signalling pathway attenuated oxidative stress and apoptosis in models of Alzheimer's disease, Parkinson's disease and intracerebral haemorrhage . More importantly, oxidative stress and apoptosis were common molecular abnormalities induced by TBI.…”

Section: Introductionmentioning

confidence: 99%

Hydrogen exerts neuroprotection by activation of the miR‐21/PI3K/AKT/GSK‐3β pathway in an in vitro model of traumatic brain injury

Wang

Yin

Wang

et al. 2020

J Cellular Molecular Medi

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Few studies have explored the effect of hydrogen on neuronal apoptosis or impaired nerve regeneration after traumatic brain injury, and the mechanisms involved in these processes are unclear. In this study, we explored neuroprotection of hydrogen‐rich medium through activation of the miR‐21/PI3K/AKT/GSK‐3β pathway in an in vitro model of traumatic brain injury. Such model adopted PC12 cells with manual scratching. Then, injured cells were cultured in hydrogen‐rich medium for 48 hours. Expression of miR‐21, p‐PI3K, p‐Akt, p‐GSK‐3β, Bax and Bcl‐2 was measured using RT‐qPCR, Western blot analysis and immunofluorescence staining. Rate of apoptosis was determined using TUNEL staining. Neuronal regeneration was assessed using immunofluorescence staining. The results showed that hydrogen‐rich medium improved neurite regeneration and inhibited apoptosis in the injured cells. Scratch injury was accompanied by up‐regulation of miR‐21, p‐PI3K, p‐Akt and p‐GSK‐3β. A miR‐21 antagomir inhibited the expression of these four molecules, while a PI3K blocker only affected the three proteins and not miR‐21. Both the miR‐21 antagomir and PI3K blocker reversed the protective effect of hydrogen. In conclusion, hydrogen exerted a neuroprotective effect against neuronal apoptosis and impaired nerve regeneration through activation of miR‐21/PI3K/AKT/GSK‐3β signalling in this in vitro model of traumatic brain injury.

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“…It is well-defined that flavonoids can act as antioxidants by themselves, because they have ROS scavenging activity, which is derived from their chemical feature ( Figure 2 ) [ 36 , 41 , 122 ]. Additionally, flavonoids can control the redox imbalance by regulating the antioxidant enzyme gene expression via Nrf2/ARE (nuclear erythroid 2-related factor 2/antioxidant response element) signaling pathway [ 144 , 145 ], and the activity of multiple cellular signaling pathways, such as Extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) [ 42 , 146 , 147 ], c-Jun N-terminal kinases (JNK) [ 146 , 148 ], phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) [ 42 , 138 , 149 ], and mitogen-activated protein kinase (p38 MAPK) signaling pathway [ 148 , 150 ]. Moreover, flavonoids can suppress apoptosis and excessive inflammatory responses, thereby reducing the ROS that is incidentally generated by the activation of a cytotoxic mechanism ( Figure 2 ) [ 43 , 138 , 151 , 152 , 153 , 154 , 155 ].…”

Section: Natural Antioxidants: Flavonoidsmentioning

confidence: 99%

Control of Reactive Oxygen Species for the Prevention of Parkinson’s Disease: The Possible Application of Flavonoids

et al. 2020

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Oxidative stress reflects an imbalance between the production of reactive oxygen species (ROS) and antioxidant defense systems, and it can be associated with the pathogenesis and progression of neurodegenerative diseases such as multiple sclerosis, stroke, and Parkinson’s disease (PD). The application of antioxidants, which can defend against oxidative stress, is able to detoxify the reactive intermediates and prevent neurodegeneration resulting from excessive ROS production. There are many reports showing that numerous flavonoids, a large group of natural phenolic compounds, can act as antioxidants and the application of flavonoids has beneficial effects in the adult brain. For instance, it is well known that the long-term consumption of the green tea-derived flavonoids catechin and epigallocatechin gallate (EGCG) can attenuate the onset of PD. Also, flavonoids such as ampelopsin and pinocembrin can inhibit mitochondrial dysfunction and neuronal death through the regulation of gene expression of the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway. Additionally, it is well established that many flavonoids exhibit anti-apoptosis and anti-inflammatory effects through cellular signaling pathways, such as those involving (ERK), glycogen synthase kinase-3β (GSK-3β), and (Akt), resulting in neuroprotection. In this review article, we have described the oxidative stress involved in PD and explained the therapeutic potential of flavonoids to protect the nigrostriatal DA system, which may be useful to prevent PD.

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Effects and mechanism of epigallocatechin-3-gallate on apoptosis and mTOR/AKT/GSK-3β pathway in substantia nigra neurons in Parkinson rats

Cited by 25 publications

References 25 publications

Metal Chelation Therapy and Parkinson’s Disease: A Critical Review on the Thermodynamics of Complex Formation between Relevant Metal Ions and Promising or Established Drugs

Metal Chelation Therapy and Parkinson’s Disease: A Critical Review on the Thermodynamics of Complex Formation between Relevant Metal Ions and Promising or Established Drugs

Hydrogen exerts neuroprotection by activation of the miR‐21/PI3K/AKT/GSK‐3β pathway in an in vitro model of traumatic brain injury

Control of Reactive Oxygen Species for the Prevention of Parkinson’s Disease: The Possible Application of Flavonoids

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