Patients with first-in-life stroke were analysed according to: plasma concentration of the following markers on the first day of stroke: interleukin 2 (IL-2) and interleuki 6 (IL-6), S100B, tumor necrosis factor-α (TNF-α), progranulin (GRN), neuron specific enolase (NSE), urokinase-type plasminogen activator (uPA), vascular endothelial growth factor (VEGF), brain-derived neurotrophic factor (BDNF), C-reactive protein (CRP), leucocyte and thrombocyte counts; their neurological status on the first day of stroke (NIHSS) and their functional status at 30 days following stroke (mRS).
We investigated whether gradual increases in tumor necrosis factor-alpha (TNF-alpha) reported during exercise down-regulates expression of TNF-alpha receptors I and II (TNFRI and II) in stroke, leading to reduced brain damage.
We also subjected TNF knockout mice to experimental stroke (permanent middle cerebral artery occlusion) and validated the effect of TNF inhibition on EV release.
Tumor necrosis factor (TNF) has been shown to be involved in the pathogenesis of hemorrhagic stroke, having deleterious effects on cerebral arteries by promoting inflammation and apoptosis in vascular and immune cells.
Possession of the TNF-alpha T allele significantly increases the risk of vascular dementia, and increases the risk of Alzheimer's disease associated with apolipoprotein E. Although further research is needed, these findings suggest a potential role for anti-inflammatory therapy in vascular dementia and Alzheimer's disease, and perhaps especially in patients who have had a stroke.
Primary rat neuronal cells were subjected to a 90-minute HBOT treatment at 2.5 absolute atmospheres prior to either tumor necrosis factor-alpha (TNF-alpha) or lipopolysaccharide (LPS) injury to simulate the inflammation-plagued secondary cell death associated with stroke and traumatic brain injury (TBI).
Injection of lentiviral miR-126-5p improved behavioral outcomes at 3 days after stroke (<i>P</i><0.05). miR-126-3p and -5p overexpression downregulated the expression of proinflammatory cytokines IL-1β and TNF-α and adhesion molecules VCAM-1 and E-selectin, as well as decreased MPO<sup>+</sup> (myeloperoxidase positive) cell numbers at 3 days after ischemia (<i>P</i><0.05).
Alveolar macrophages and epithelial and endothelial cells of Sham and Stroke animals were also isolated for evaluation of mRNA expression of interleukin (IL)-6 and tumor necrosis factor (TNF)-α.
This work was designed to examine the effect of mouse recombinant resistin on mRNA expression of Tumor necrosis factor-α (TNF-α), Interleukin-1β (IL-1β), Interleukin-10 (IL-10), Transforming growth factor-β1 (TGF- β1), and Heat shock protein-70 (HSP-70) in mouse model of stroke.
Following multivariate adjustment, carriers of the TNF-alpha (-308)A allele, the IL-1-RA 2* allele or the IL-6 (-174)C allele appeared to have an increased risk of stroke in association with a febrile episode prior to strokes.
The aim of this replication study was to confirm our previous findings of associations between the TNF(-308) G/A, IL4R 503 S/P, and ADRB2 27 Q/E polymorphisms and large vessel stroke risk.
Susceptibility for ischemic stroke in Korean population is associated with polymorphisms of the interleukin-1 receptor antagonist and tumor necrosis factor-alpha genes, but not the interleukin-1beta gene.