scholarly journals Dimethyl fumarate attenuates experimental autoimmune neuritis through the nuclear factor erythroid-derived 2-related factor 2/hemoxygenase-1 pathway by altering the balance of M1/M2 macrophages

2016 ◽  
Vol 13 (1) ◽  
Author(s):  
Ranran Han ◽  
Jinting Xiao ◽  
Hui Zhai ◽  
Junwei Hao
Keyword(s):  
Dimethyl Fumarate ◽  
Related Factor ◽  
Experimental Autoimmune Neuritis ◽  
Nuclear Factor ◽  
M2 Macrophages ◽  
Experimental Autoimmune

Neuroprotective effect of dimethyl fumarate in stroke: The role of nuclear factor erythroid 2-related factor 2

2019 ◽  
Author(s):  
Anahid Safari ◽  
Hamzeh Badeli-Sarkala2 ◽  
Mohammad Reza Namavar ◽  
Elias Kargar-Abarghouei ◽  
Neda Anssari ◽  
...  
Keyword(s):  
Middle Cerebral Artery ◽  
Infarct Volume ◽  
Dimethyl Fumarate ◽  
Treated Group ◽  
Vehicle Group ◽  
Related Factor ◽  
Nuclear Factor ◽  
Neuroprotective Effects ◽  
Total Brain ◽  
Nrf2 Expression

Background: There is evidence that supports the neuroprotective effects of dimethyl fumarate (DMF) in stroke. Nuclear factor erythroid 2-related factor 2 (Nrf2) has both anti-oxidant and anti-inflammatory mechanisms. We investigated the neuroprotective effects of DMF via Nrf2 activation in the cortex, striatum, and diencephalon in a middle cerebral artery occlusion (MCAO) model of stroke. Methods: 22 Sprague-Dawley male rats were randomized into 3 groups. In DMF-treated group (n = 8), rats received 15 mg/kg oral DMF twice daily by gavage from day 0 to 14 after a 60-minute MCAO. The vehicle group (n = 7) underwent MCAO and were given methocel/H2O, using the same method and schedule. In the sham group (n = 7), neck was opened, but neither middle cerebral artery (MCA) was occluded nor any drug was administered. After 14 days, the animals were sacrificed. The infarct volume were assessed by stereology method. Nrf2 expression was evaluated in the cortex, striatum, and diencephalon by immunohistochemistry method. Results: Ratio of infarct to total brain volume was significantly lower in the DMF-treated group (5.76%) in comparison with the vehicle group (22.39%) (P < 0.0001). Nrf2 expression was higher in DMFtreated group in comparison with both the vehicle and sham groups in cortex, striatum, diencephalon, and total brain (P < 0.0001). In the DMF-treated group, significant negative correlation between Nrf2 expression and infarct volume was observed in cortex, striatum, diencephalon, and total brain. Conclusion: DMF induces Nrf2 expression and its neuroprotective effects in different brain anatomical regions.  

scholarly journals Antioxidant and Anti-inflammatory Effect of Nrf2 Inducer Dimethyl Fumarate in Neurodegenerative Diseases

Antioxidants ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 630 ◽  
Author(s):  
Sarah A. Scuderi ◽  
Alessio Ardizzone ◽  
Irene Paterniti ◽  
Emanuela Esposito ◽  
Michela Campolo
Keyword(s):  
Oxidative Stress ◽  
Neurodegenerative Diseases ◽  
Fumaric Acid ◽  
Dimethyl Fumarate ◽  
Related Factor ◽  
Nuclear Factor ◽  
Beneficial Effects ◽  
Anti Inflammatory

Neurodegenerative diseases (NDs) represents debilitating conditions characterized by degeneration of neuronal cells in specific brain areas, causing disability and death in patients. In the pathophysiology of NDs, oxidative stress, apoptosis and neuroinflammation have a key role, as demonstrated by in vivo and in vitro models. Therefore, the use of molecules with antioxidant and anti-inflammatory activities represents a possible strategy for the treatment of NDs. Many studies demonstrated the beneficial effects of fumaric acid esters (FAEs) to counteract neuroinflammation and oxidative stress. Among these molecules, dimethyl fumarate (DMF) showed a valid therapeutic approach to slow down neurodegeneration and relieve symptoms in patients with NDs. DMF is a methyl ester of fumaric acid and acts as modulator of the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway as well as nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) translocation. Therefore, this review aims to examine the potential beneficial effects of DMF to counteract oxidative stress and inflammation in patients with NDs.

scholarly journals Dimethyl Fumarate Ameliorates Lewis Rat Experimental Autoimmune Neuritis and Mediates Axonal Protection

PLoS ONE ◽  
2015 ◽  
Vol 10 (11) ◽  
pp. e0143416 ◽  
Author(s):  
Kalliopi Pitarokoili ◽  
Björn Ambrosius ◽  
Daniela Meyer ◽  
Lisa Schrewe ◽  
Ralf Gold
Keyword(s):  
Dimethyl Fumarate ◽  
Experimental Autoimmune Neuritis ◽  
Lewis Rat ◽  
Experimental Autoimmune

scholarly journals Protective Role of Nuclear Factor E2-Related Factor 2 against Acute Oxidative Stress-Induced Pancreaticβ-Cell Damage

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Jingqi Fu ◽  
Hongzhi Zheng ◽  
Huihui Wang ◽  
Bei Yang ◽  
Rui Zhao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Damage ◽  
Dimethyl Fumarate ◽  
Protective Role ◽  
Related Factor ◽  
Dependent Manner ◽  
Nuclear Factor ◽  
Min6 Cells ◽  
Cell Dysfunction ◽  
Glucose Stimulated Insulin Secretion

Oxidative stress is implicated in the pathogenesis of pancreaticβ-cell dysfunction that occurs in both type 1 and type 2 diabetes. Nuclear factor E2-related factor 2 (NRF2) is a master regulator in the cellular adaptive response to oxidative stress. The present study found that MIN6β-cells with stable knockdown ofNrf2(Nrf2-KD) and islets isolated fromNrf2-knockout mice expressed substantially reduced levels of antioxidant enzymes in response to a variety of stressors. In scramble MIN6 cells or wild-type islets, acute exposure to oxidative stressors, including hydrogen peroxide (H2O2) and S-nitroso-N-acetylpenicillamine, resulted in cell damage as determined by decrease in cell viability, reduced ATP content, morphology changes of islets, and/or alterations of apoptotic biomarkers in a concentration- and/or time-dependent manner. In contrast, silencing ofNrf2sensitized MIN6 cells or islets to the damage. In addition, pretreatment of MIN6β-cells with NRF2 activators, including CDDO-Im, dimethyl fumarate (DMF), andtert-butylhydroquinone (tBHQ), protected the cells from high levels of H2O2-induced cell damage. Given that reactive oxygen species (ROS) are involved in regulating glucose-stimulated insulin secretion (GSIS) and persistent activation of NRF2 blunts glucose-triggered ROS signaling and GSIS, the present study highlights the distinct roles that NRF2 may play in pancreaticβ-cell dysfunction that occurs in different stages of diabetes.

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