TNF, tumor necrosis factor, 7124

N. diseases: 2724; N. variants: 31
Source: ALL
Disease Score gda Association Type Type Original DB Sentence supporting the association PMID PMID Year
CUI: C0740391
Disease: Middle Cerebral Artery Occlusion
Middle Cerebral Artery Occlusion
0.100 AlteredExpression disease BEFREE In this work, male rats were treated with JNK-IN-8 after transient middle cerebral artery occlusion, and then the modified improved neurological function score (mNSS), the foot-fault test (FFT), interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) levels were assessed. 31541462 2020
CUI: C0740391
Disease: Middle Cerebral Artery Occlusion
Middle Cerebral Artery Occlusion
0.100 AlteredExpression disease BEFREE Expression of Iba1, tumor necrosis factor-α, interleukin-1β and interleukin-6 was significantly lower in the acacetin group compared with the middle cerebral artery occlusion group. 30632500 2019
CUI: C0740391
Disease: Middle Cerebral Artery Occlusion
Middle Cerebral Artery Occlusion
0.100 AlteredExpression disease BEFREE <b>Results:</b> MCAo resulted in profound attenuation of immune activation, as anticipated. t-PA treatment not only worsened neurological deficit, but further reduced lymphocyte and monocyte counts in blood, enhanced plasma levels of both IL-10 and TNFα and decreased various conventional DC subsets in the spleen and cLN, consistent with enhanced immunosuppression and systemic inflammation after stroke. 30972077 2019
CUI: C0740391
Disease: Middle Cerebral Artery Occlusion
Middle Cerebral Artery Occlusion
0.100 Biomarker disease BEFREE Furthermore, reducing Trim47 apparently decreased the release of pro-inflammatory factors, including interleukin 6 (IL-6), tumor necrosis factor-α (TNF-α) and inducible nitric oxide synthase (iNOS), in brain samples of MCAO rats, which was partly by the blockage of nuclear factor-kappa B (NF-κB) signaling. 31178138 2019
CUI: C0740391
Disease: Middle Cerebral Artery Occlusion
Middle Cerebral Artery Occlusion
0.100 Biomarker disease BEFREE Following middle cerebral artery occlusion/reperfusion (MCAO/R) surgery, rats were treated orally with 32, 16, and 8 mg/kg AR respectively for 14 days during which cerebral injury was evaluated and proinflammatory factors tumor necrosis factor-α and interleukin-6 as well as neurotrophic factors brain-derived neurotrophic factor and Neurotrophin-3 levels were determined with ELISA kits. 31395423 2019
CUI: C0740391
Disease: Middle Cerebral Artery Occlusion
Middle Cerebral Artery Occlusion
0.100 AlteredExpression disease BEFREE BV2 cells under OGD for 0, 6, 12, or 24 h exhibited decreased USP18 expression and increased expression of the proinflammatory cytokines including interleukin (IL)-1β, IL-6, IL-8, tumor necrosis factor (TNF)-α, and interferon (INF)-γ. Lentiviral overexpression of USP18 in MCAO mice significantly decreased the infarct volume and significantly increased the number of new neurons that coexpressed bromodeoxyuridine (BrdU)/neuronal nuclei (NeuN). 31513843 2019
CUI: C0740391
Disease: Middle Cerebral Artery Occlusion
Middle Cerebral Artery Occlusion
0.100 Biomarker disease BEFREE The combined administration also regulates the IL-1β and TNF-α in the MCAO rat peripheral blood and ameliorate the brain damage in MCAO rats. 29258757 2018
CUI: C0740391
Disease: Middle Cerebral Artery Occlusion
Middle Cerebral Artery Occlusion
0.100 AlteredExpression disease BEFREE The mRNA expression levels of nod-like receptor protein 3 (NLRP3), tumor necrosis factor alpha (TNF-α), and interleukin-6 (IL-6) and protein expression levels of NLRP3 were assessed. l-Homocarnosine supplementation substantially increased SOD, catalase, Gpx, and GSH levels, whereas it reduced the levels of lipid peroxidation relative to MCAO rats. l-Homocarnosine significantly reduced the infarct area and neurological deficit score, as well as histopathological alteration, apoptosis, and necrosis in brain tissue. 29890246 2018
CUI: C0740391
Disease: Middle Cerebral Artery Occlusion
Middle Cerebral Artery Occlusion
0.100 Biomarker disease BEFREE The inflammatory cytokines tumor necrosis factor-α (TNFα), interleukin (IL)-1β, and IL-6 of mouse brains after MCAO and BV2 cells treated with oxygen-glucose deprivation were measured using enzyme-linked immunosorbent assay, and apoptotic proteins were examined by Western blotting. 30497184 2018
CUI: C0740391
Disease: Middle Cerebral Artery Occlusion
Middle Cerebral Artery Occlusion
0.100 AlteredExpression disease BEFREE A significant elevation on serum levels of TNF-α and IL-6 was noted with MCAO which was markedly reduced by TFD. 30430924 2018
CUI: C0740391
Disease: Middle Cerebral Artery Occlusion
Middle Cerebral Artery Occlusion
0.100 Biomarker disease BEFREE In a murine middle cerebral artery occlusion (MCAO) stroke model, HNG ameliorates cerebral infarction and suppresses the production of TNF-α, IL-1β, IL-6 and MCP-1 cytokines. 29999240 2018
CUI: C0740391
Disease: Middle Cerebral Artery Occlusion
Middle Cerebral Artery Occlusion
0.100 AlteredExpression disease BEFREE The results of enzyme-linked immunosorbent assay (ELISA) showed that perampanel significantly decreased the expression of pro-inflammatory cytokines IL-1β and TNF-α, whereas it increased the levels of anti-inflammatory cytokines IL-10 and TGF-β1 after MCAO. 28401316 2018
CUI: C0740391
Disease: Middle Cerebral Artery Occlusion
Middle Cerebral Artery Occlusion
0.100 Biomarker disease BEFREE We also subjected TNF knockout mice to experimental stroke (permanent middle cerebral artery occlusion) and validated the effect of TNF inhibition on EV release. 29807527 2018
CUI: C0740391
Disease: Middle Cerebral Artery Occlusion
Middle Cerebral Artery Occlusion
0.100 AlteredExpression disease BEFREE Endogenous expressions of Gas6 and Axl decreased significantly by 24h after MCAO. rGas6 reduced brain infarction and improved neurologic deficits scores, and increased expression of Axl and decreased the expressions of TRAF3, TRAF6 and inflammatory factors IL-1β, IL-6, and TNF-α. 29196212 2018
CUI: C0740391
Disease: Middle Cerebral Artery Occlusion
Middle Cerebral Artery Occlusion
0.100 Biomarker disease BEFREE The concentrations of TNF‑α, interleukin (IL)‑1β, IL‑6, and HMGB1 in the group treated with STAT3 inhibitor (MCAO + rapamycin), JAK2 inhibitor (MCAO + AG490), and MCAO + curcumin were significantly lower than in the MCAO group (P<0.01), as well as the relative content of p‑JAK2/JAK2 and p‑STAT3/STAT3 (P<0.05). 29393445 2018
CUI: C0740391
Disease: Middle Cerebral Artery Occlusion
Middle Cerebral Artery Occlusion
0.100 AlteredExpression disease BEFREE Tumor necrosis factor-α and IL-1β mRNA expression markedly increased at 12-hour time point and then returned to the basal level at 24 hours after MCAO; but HSP-70 mRNA expression increased at 24-hour time point. 30120034 2018
CUI: C0740391
Disease: Middle Cerebral Artery Occlusion
Middle Cerebral Artery Occlusion
0.100 Biomarker disease BEFREE In addition, vitexin attenuated the secretion of pro-inflammatory cytokine (interleukin (IL)-6 and tumor necrosis factor alpha (TNF-?)) and increased anti-inflammatory cytokine (IL-10) production to ameliorate MCAO-induced inflammation. 29710456 2018
CUI: C0740391
Disease: Middle Cerebral Artery Occlusion
Middle Cerebral Artery Occlusion
0.100 Biomarker disease BEFREE Western blot analysis shows that vasculotide significantly decreases expression of receptor for advanced glycation end products (RAGE), MCP-1 and TNF-α in the ischemic brain compared with T1DM-MCAo rats. 30124060 2018
CUI: C0740391
Disease: Middle Cerebral Artery Occlusion
Middle Cerebral Artery Occlusion
0.100 AlteredExpression disease BEFREE A significant elevation on serum levels of TNF-α and IL-6 was noted with MCAO which was markedly reduced by TFD. 30457456 2018
CUI: C0740391
Disease: Middle Cerebral Artery Occlusion
Middle Cerebral Artery Occlusion
0.100 AlteredExpression disease BEFREE Furthermore, the IN group had lower expression of interleukin-1β and tumor necrosis factor-α at 6 h after MCAO than the EC group (<i>p</i><0.05). 27530114 2017
CUI: C0740391
Disease: Middle Cerebral Artery Occlusion
Middle Cerebral Artery Occlusion
0.100 Biomarker disease BEFREE Lig also could effectively decrease the levels of interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in serum and brain tissues of the MCAO rats. 28455258 2017
CUI: C0740391
Disease: Middle Cerebral Artery Occlusion
Middle Cerebral Artery Occlusion
0.100 AlteredExpression disease BEFREE Moreover, other important events were observed in MCAO+RIPC group, including substantial decrements in the concentrations of oxidative response indicators [malondialdehyde (MDA), 8-hydroxy-2-deoxyguanosine (8-OHdG), and protein carbonyl], significant reductions in levels of inflammation mediators [myeloperoxidase (MPO), tumor necrosis factor-a (TNF-a), interleukin-1β (IL-1β), and IL-6], and significant decline in neuronal apoptosis revealed by a smaller number of TUNEL-positive cells. 27896629 2017
CUI: C0740391
Disease: Middle Cerebral Artery Occlusion
Middle Cerebral Artery Occlusion
0.100 AlteredExpression disease BEFREE Here, we found that FK866, a potent NAMPT inhibitor, decreased the level of TNF-α, NAMPT and IL-6 in the ischemic brain tissue one day after middle-cerebral-artery occlusion and reperfusion (MCAO/R), improved neurological dysfunction, decreased infarct volume and neuronal loss, and inhibited microgliosis and astrogliosis 14days after MCAO/R. 28528966 2017
CUI: C0740391
Disease: Middle Cerebral Artery Occlusion
Middle Cerebral Artery Occlusion
0.100 Biomarker disease BEFREE The expression levels of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and transforming growth factor-β1 (TGF-β1) were increased, while the level of interleukin-10 (IL-10) was reduced in the infarct cortex 7 days after MCAO, as assessed by immunohistochemistry, western blotting and quantitative real-time PCR (qRT-PCR). 27585466 2017
CUI: C0740391
Disease: Middle Cerebral Artery Occlusion
Middle Cerebral Artery Occlusion
0.100 Biomarker disease BEFREE In an experimental mouse (C57BL/6NTac) model of middle cerebral artery occlusion (MCAO), we observed that SB mediates neuroprotection by epigenetically regulating the microglial inflammatory response, via downregulating the expression of pro-inflammatory mediators, TNF-α and NOS2, and upregulating the expression of anti-inflammatory mediator IL10, in activated microglia. 27722928 2017