ArticleNeurotoxicity research2018
Dimethyl Fumarate Limits Neuroinflammation and Oxidative Stress and Improves Cognitive Impairment After Polymicrobial Sepsis.
Article in Neurotoxicity research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 49 citations in OpenAlex.
- Assessment of methylene blue and NAD on LPS-induced acute brain injury: effects on neuroinflammation, oxidative stress, and blood-brain barrier integrity in a rat endotoxemia model.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Maternal exposure to fine particulate matter and autism spectrum disorder in children: population based case-control study.Frontiers in public health · 2026Article
- Impact of Diabetes on Oxidative Stress, Mitochondrial Function, and Neurological Outcomes Following Ischemic Stroke: A Sex-Based Experimental Analysis.Molecular neurobiology · 2025Article
- Dimethyl fumarate improves sepsis-induced acute lung injury by inhibiting STING-mediated ferroptosis.Journal of bioenergetics and biomembranes · 2025Article
- Dimethyl Fumarate Strongly Ameliorates Gray and White Matter Brain Injury and Modulates Glial Activation after Severe Hypoxia-Ischemia in Neonatal Rats.Antioxidants (Basel, Switzerland) · 2024Article
- Identification of key neuronal mechanisms triggered by dimethyl fumarate in SH-SY5Y human neuroblastoma cells through a metabolomic approach.Archives of toxicology · 2024Article
- Amelioration of Neurochemical Alteration and Memory and Depressive Behavior in Sepsis by Allopurinol, a Tryptophan 2,3-Dioxygenase Inhibitor.CNS & neurological disorders drug targets · 2024Article
- Disulfiram blocks inflammatory TLR4 signaling by targeting MD-2.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Inhibition of ITK Signaling Causes Amelioration in Sepsis-Associated Neuroinflammation and Depression-like State in Mice.International journal of molecular sciences · 2023Article
- Is Nuclear Factor Erythroid 2-Related Factor 2 a Target for the Intervention of Cytokine Storms?Antioxidants (Basel, Switzerland) · 2023Review
- PD-L1 promotes GSDMD-mediated NET release by maintaining the transcriptional activity of Stat3 in sepsis-associated encephalopathy.International journal of biological sciences · 2023Article
- Pathogenesis of sepsis-associated encephalopathy: more than blood-brain barrier dysfunction.Molecular biology reports · 2022Review
- Review
- Dimethyl fumarate improves cognitive impairment by enhancing hippocampal brain-derived neurotrophic factor levels in hypothyroid rats.BMC endocrine disorders · 2022Article
- Roles of neutrophil reactive oxygen species (ROS) generation in organ function impairment in sepsis.Journal of Zhejiang University. Science. B · 2022Review
- Emerging Trends and Hot Spots in Sepsis-Associated Encephalopathy Research From 2001 to 2021: A Bibliometric Analysis.Frontiers in medicine · 2022Article
- Current Understanding of Long-Term Cognitive Impairment After Sepsis.Frontiers in immunology · 2022Review
- NRF2 Activation Ameliorates Oxidative Stress and Improves Mitochondrial Function and Synaptic Plasticity, and in A53T α-Synuclein Hippocampal Neurons.Antioxidants (Basel, Switzerland) · 2021Article
- Dimethyl fumarate prevents acute lung injury related cognitive impairment potentially via reducing inflammation.Journal of cardiothoracic surgery · 2021Article
- Sepsis and multiple sclerosis: Causative links and outcomes.Immunology letters · 2021Review
Corrections and comments
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Authors and funding
17 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis is caused by a dysregulated host response to infection, often associated with acute central nervous system (CNS) dysfunction, which results in long-term cognitive impairment. Dimethyl fumarate (DMF) is an important agent against inflammatory response and reactive species in CNS disorders. Evaluate the effect of DMF on acute and long-term brain dysfunction after experimental sepsis in rats. Male Wistar rats were submitted to the cecal ligation and puncture (CLP) model. The groups were divided into sham (control) + vehicle, sham + NAC, sham + DMF, CLP + vehicle, CLP + NAC, and CLP + DMF. The animals were treated with DMF (15 mg/kg at 0 and 12 h after CLP, per gavage) and the administration of n-acetylcysteine (NAC) (20 mg/kg; 3, 6, and 12 h after CLP, subcutaneously) was used as positive control. Twenty-four hours after CLP, cytokines, myeloperoxidase (MPO), nitrite/nitrate (N/N), oxidative damage to lipids and proteins, and antioxidant enzymes were evaluated in the hippocampus, total cortex, and prefrontal cortex. At 10 days after sepsis induction, behavioral tests were performed to assess cognitive damage. We observed an increase in cytokine levels, MPO activity, N/N concentration, and oxidative damage, a reduction in SOD and GPx activity in the brain structures, and cognitive damage in CLP rats. DMF treatment was effective in reversing these parameters. DMF reduces sepsis-induced neuroinflammation, oxidative stress, and cognitive impairment in rats subjected to the CLP model.
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