ArticleJournal of neuroinflammation2017
Sulfosuccinimidyl oleate sodium is neuroprotective and alleviates stroke-induced neuroinflammation.
Article in Journal of neuroinflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 34 citations in OpenAlex.
- Fatty Acid Metabolism in Health and Cancer: From Fundamental Mechanisms to Therapeutic Application.MedComm · 2026Review
- TNIK as a molecular switch regulating platelet function in hemostasis and hyperlipidemia-associated thrombosis.Blood advances · 2026Article
- Distinct roles of dopamine receptors in HIV latency reversal in a myeloid cell model.Frontiers in immunology · 2026Article
- The gut-brain axis: mechanisms linking intestinal dysbiosis with stroke.Frontiers in cell and developmental biology · 2026Review
- Review
- Inhibition of CD36 ameliorates mouse spinal cord injury by accelerating microglial lipophagy.Acta pharmacologica Sinica · 2025Article
- CD36 deletion prevents white matter injury by modulating microglia polarization through the Traf5-MAPK signal pathway.Journal of neuroinflammation · 2024Article
- Role of CD36 in central nervous system diseases.Neural regeneration research · 2024Review
- Sulfosuccinimidyl oleate ameliorates the high-fat diet-induced obesity syndrome by reducing intestinal and hepatic absorption.Frontiers in pharmacology · 2023Article
- Ferroptosis and mitochondrial dysfunction in acute central nervous system injury.Frontiers in cellular neuroscience · 2023Review
- Review
- Low-Concentrations of Fatty Acids Induce an Early Increase in IL-8 Levels in Normal Human Astrocytes.Metabolites · 2022Article
- Taurolithocholic acid but not tauroursodeoxycholic acid rescues phagocytosis activity of bone marrow-derived macrophages under inflammatory stress.Journal of cellular physiology · 2022Article
- Article
- Arginine is neuroprotective through suppressing HIF-1α/LDHA-mediated inflammatory response after cerebral ischemia/reperfusion injury.Molecular brain · 2020Article
- Dectin-1/Syk signaling triggers neuroinflammation after ischemic stroke in mice.Journal of neuroinflammation · 2020Article
- Immune Cells After Ischemic Stroke Onset: Roles, Migration, and Target Intervention.Journal of molecular neuroscience : MN · 2018Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIschemic stroke is one of the main causes of death and disability worldwide. It is caused by the cessation of cerebral blood flow resulting in the insufficient delivery of glucose and oxygen to the neural tissue. The inflammatory response initiated by ischemic stroke in order to restore tissue homeostasis in the acute phase of stroke contributes to delayed brain damage.
methodsBy using in vitro models of neuroinflammation and in vivo model of permanent middle cerebral artery occlusion, we demonstrate the neuroprotective and anti-inflammatory effects of sulfosuccinimidyl oleate sodium (SSO).
resultsSSO significantly reduced the lipopolysaccharide/interferon-γ-induced production of nitric oxide, interleukin-6 and tumor necrosis factor-α, and the protein levels of inflammatory enzymes including nitric oxide synthase 2, cyclooxygenase-2 (COX-2), and p38 mitogen-activated protein kinase (MAPK) in microglia, without causing cell toxicity. Although SSO failed to directly alleviate glutamate-induced excitotoxicity in murine cortical neurons, it prevented inflammation-induced neuronal death in microglia-neuron co-cultures. Importantly, oral administration of SSO in Balb/c mice subjected to permanent occlusion of the middle cerebral artery reduced microglial activation in the peri-ischemic area and attenuated brain damage. This in vivo neuroprotective effect of SSO was associated with a reduction in the COX-2 and heme oxygenase-1 immunoreactivities.
conclusionsOur results suggest that SSO is an anti-inflammatory and a possible therapeutic candidate in diseases such as stroke where inflammation is a central hallmark.
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