Dimethyl Fumarate Mitigates Tauopathy in Aβ-Induced Neuroblastoma SH-SY5Y Cells

Rajput, Mithun Singh; Nirmal, Nilesh Prakash; Rathore, Devashish; Dahima, Rashmi

doi:10.1007/s11064-020-03115-x

Cited by 12 publications

(4 citation statements)

References 43 publications

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“…Considering the aim of our study, we do not correlate the increase of phospho-AKT protein levels to HO-1 up-regulation nor we included data regarding the effects of PD98059 in co-treated SIRC with DMF and high glucose, as we included DMF as positive control. However, this data is certainly in agreement with the HO-1 inducer activity of DMF mediated by phospho-AKT and observed in other models [ 35 , 62 , 63 ]. Reported data indicate that different compounds induce Nrf2/HO-1 axis in hyperglycemia-stimulated epithelial cells through the involvement of both Akt and ERK 1/2 signaling [ 15 , 64 ].…”

Section: Discussionsupporting

confidence: 92%

Glucose-Impaired Corneal Re-Epithelialization Is Promoted by a Novel Derivate of Dimethyl Fumarate

et al. 2021

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Glucose induces corneal epithelial dysfunctions characterized by delayed wound repair. Nuclear erythroid 2-related factor 2 (Nrf2) mediates cell protection mechanisms even through the Heme oxygenase-1 (HO-1) up-regulation. Here, we synthesized new HO-1 inducers by modifying dimethyl fumarate (DMF) and used docking studies to select VP13/126 as a promising compound with the best binding energy to Kelch-like ECH-associated protein 1 (keap1), which is the the regulator of Nrf2 nuclear translocation. We verified if VP13/126 protects SIRC cells from hyperglycemia compared to DMF. SIRC were cultured in normal (5 mM) or high glucose (25 mM, HG) in presence of DMF (1–25 μM) or VP13/126 (0.1–5 μM) with or without ERK1/2 inhibitor PD98059 (15 μM). VP13/126 was more effective than DMF in the prevention of HG-induced reduction of cell viability and proliferation. Reduction of wound closure induced by HG was similarly counteracted by 1 μM VP13/126 and 10 μM DMF. VP13/126 strongly increased phospho/total ERK1/2 and restored HO-1 protein in HG-treated SIRC; these effects are completely counteracted by PD98059. Moreover, high-content screening analysis showed a higher rate of Nrf2 nuclear translocation induced by VP13/126 than DMF in HG-stimulated SIRC. These data indicate that VP13/126 exerts remarkable pro-survival properties in HG-stimulated SIRC, promoting the Nrf2/HO-1 axis.

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Section: Discussionsupporting

confidence: 92%

Glucose-Impaired Corneal Re-Epithelialization Is Promoted by a Novel Derivate of Dimethyl Fumarate

et al. 2021

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“…The accumulation of amyloid beta peptides gets deposited in the brain as plaques, and the loss of cholinergic neurons leads to AD pathogenesis ( Rajput et al, 2020b ). Inhibition of cholinesterases (butyrylcholinesterase (BChE) and acetylcholinesterase (AChE)) that degrade neurotransmitters is crucial ( Moussa-Pacha et al, 2020 , Rajput et al, 2020a ).…”

Section: Discussionmentioning

confidence: 99%

Phenolic content of Thai Bao mango peel and its in-vitro antioxidant, anti-cholinesterase, and antidiabetic activities

Thangsiri,

Suttisansanee,

Koirala

et al. 2024

Saudi Journal of Biological Sciences

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“…Furthermore, DMF also mitigates tauopathy in Aβtreated cell models. DMF pretreatment suppressed tau phosphorylation at Ser396 and Aβ 1-42 -induced Thr231 by reducing the activity of GSK-3β in cells to inhibit NFT formation (Rajput et al, 2020).…”

Section: Synthetic Compoundsmentioning

confidence: 99%

Iron dyshomeostasis and ferroptosis in Alzheimer’s disease: Molecular mechanisms of cell death and novel therapeutic drugs and targets for AD

2022

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Alzheimer’s disease (AD) is a degenerative disease of the central nervous system that is the most common type of senile dementia. Ferroptosis is a new type of iron-dependent programmed cell death identified in recent years that is different from other cell death forms. Ferroptosis is induced by excessive accumulation of lipid peroxides and reactive oxygen species (ROS) in cells. In recent years, it has been found that ferroptosis plays an important role in the pathological process of AD. Iron dyshomeostasis contribute to senile plaques (SP) deposition and neurofibrillary tangles (NFTs). Iron metabolism imbalance in brain and the dysfunction of endogenous antioxidant systems including system Xc- and glutathione peroxidase (GPX) are closely related to the etiopathogenesis of AD. Dysfunction of nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy induced ferroptosis can accelerates the pathological process of AD. In addition, NRF2, through regulating the expression of a considerable number of genes related to ferroptosis, including genes related to iron and glutathione metabolism, plays an important role in the development of AD. Here, we review the potential interaction between AD and ferroptosis and the major pathways regulating ferroptosis in AD. We also review the active natural and synthetic compounds such as iron chelators, lipid peroxidation inhibitors and antioxidants available to treat AD by alleviating iron dyshomeostasis and preventing ferroptosis in mice and cell models to provide valuable information for the future treatment and prevention of AD.

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Dimethyl Fumarate Mitigates Tauopathy in Aβ-Induced Neuroblastoma SH-SY5Y Cells

Cited by 12 publications

References 43 publications

Glucose-Impaired Corneal Re-Epithelialization Is Promoted by a Novel Derivate of Dimethyl Fumarate

Glucose-Impaired Corneal Re-Epithelialization Is Promoted by a Novel Derivate of Dimethyl Fumarate

Phenolic content of Thai Bao mango peel and its in-vitro antioxidant, anti-cholinesterase, and antidiabetic activities

Iron dyshomeostasis and ferroptosis in Alzheimer’s disease: Molecular mechanisms of cell death and novel therapeutic drugs and targets for AD

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