PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 14764603-6 2004 Moreover, TNF-alpha produced inhibitor kappaB kinase (IKK)-beta activation and inhibitor kappaB-beta and -alpha degradation in a p38 MAPK-dependent manner, and treatment with salicylate (an inhibitor of IKK) completely restored insulin signaling. Salicylates 175-185 tumor necrosis factor Rattus norvegicus 10-19 17911533-0 2008 Salicylate blocks lipolytic actions of tumor necrosis factor-alpha in primary rat adipocytes. Salicylates 0-10 tumor necrosis factor Rattus norvegicus 39-66 17911533-6 2008 To elucidate the cellular basis of this action, we show that salicylate suppresses TNF-alpha-induced extracellular signal-related kinase activation and intracellular cAMP elevation, two early events during the lipolysis response to TNF-alpha. Salicylates 61-71 tumor necrosis factor Rattus norvegicus 83-92 17911533-6 2008 To elucidate the cellular basis of this action, we show that salicylate suppresses TNF-alpha-induced extracellular signal-related kinase activation and intracellular cAMP elevation, two early events during the lipolysis response to TNF-alpha. Salicylates 61-71 tumor necrosis factor Rattus norvegicus 232-241 17911533-9 2008 TNF-alpha down-regulates perilipin but promotes its phosphorylation during lipolysis stimulation; these actions are efficiently reversed by salicylate. Salicylates 140-150 tumor necrosis factor Rattus norvegicus 0-9 17911533-10 2008 Salicylate slightly reduces basal but completely inhibits TNF-alpha-liberated lipase activity. Salicylates 0-10 tumor necrosis factor Rattus norvegicus 58-67 17911533-13 2008 These results provide novel evidence that salicylate directly blocks TNF-alpha-mediated FFA efflux from adipocytes, hence reducing plasma FFA levels and increasing insulin sensitivity. Salicylates 42-52 tumor necrosis factor Rattus norvegicus 69-78 10357911-9 1999 Salicylate, but not ibuprofen, significantly reduced TNF-alpha production in LPS-stimulated macrophages. Salicylates 0-10 tumor necrosis factor Rattus norvegicus 53-62 14764603-7 2004 Furthermore, TNF-alpha produced serine phosphorylation of IR and IRS-1 (total and on Ser(307) residue), and these effects were completely precluded by pretreatment with either PD169316 or salicylate. Salicylates 188-198 tumor necrosis factor Rattus norvegicus 13-22 12934647-3 2003 Salicylate inhibited the IL-1beta and TNF-alpha-induced COX-2 expressions, regulated the activation of ERK, IKK and IkappaB degradation, and the subsequent activation of NF-kappaB, in neonatal rat ventricular cardiomyocytes. Salicylates 0-10 tumor necrosis factor Rattus norvegicus 38-47 8620595-7 1996 TNF, either alone or combined with IFN, significantly stimulated prostaglandin E2, which was inhibited by either salicylate (4 mmol/L) or indomethacin (25 mumol/L). Salicylates 113-123 tumor necrosis factor Rattus norvegicus 0-3 8620595-8 1996 Salicylate, when given either before or after IFN + TNF, reduced mRNA levels of iNOS induced by cytokines. Salicylates 0-10 tumor necrosis factor Rattus norvegicus 52-55 24092407-5 2014 GPIAS showed that rats with long-term administration of salicylate were experiencing tinnitus, and the mRNA and protein expression levels of TNF-alpha and NR2A were up-regulated in chronic treatment groups, and they returned to baseline 14 days after cessation of treatment. Salicylates 56-66 tumor necrosis factor Rattus norvegicus 141-150 24092407-7 2014 These data revealed that chronic salicylate administration markedly, but reversibly, induces tinnitus possibly via augmentation of the expression of TNF-alpha and NR2A and cause changes in synaptic ultrastructure in the CN. Salicylates 33-43 tumor necrosis factor Rattus norvegicus 149-158 31495078-6 2019 Similarly, expression of the inflammatory cytokine genes TNFalpha and immediate-early gene ARC was significantly increased in the salicylate-treated cells, and decreased when the cells were treated with memantine. Salicylates 130-140 tumor necrosis factor Rattus norvegicus 57-65 28849125-6 2017 The expression of TNF-alpha and NR2A genes were increased in the auditory cortex (AC) following long-term administration of salicylate, whereas the expression of IFN-gamma genes decreased; however, the mRNA levels reversed back to normal baseline 14 days following the cease of salicylate administration. Salicylates 124-134 tumor necrosis factor Rattus norvegicus 18-27 28849125-6 2017 The expression of TNF-alpha and NR2A genes were increased in the auditory cortex (AC) following long-term administration of salicylate, whereas the expression of IFN-gamma genes decreased; however, the mRNA levels reversed back to normal baseline 14 days following the cease of salicylate administration. Salicylates 278-288 tumor necrosis factor Rattus norvegicus 18-27 27130437-6 2016 Both salicylate and 2,6 dihydroxybenzoic acid suppressed TNFalpha-induced IkappaB degradation, and in genetic knockout experiments, we found that the effect of salicylate on IkappaB degradation was AMPK-independent. Salicylates 5-15 tumor necrosis factor Rattus norvegicus 57-65 27130437-6 2016 Both salicylate and 2,6 dihydroxybenzoic acid suppressed TNFalpha-induced IkappaB degradation, and in genetic knockout experiments, we found that the effect of salicylate on IkappaB degradation was AMPK-independent. Salicylates 160-170 tumor necrosis factor Rattus norvegicus 57-65 25874611-8 2015 Data demonstrated that salicylate significantly improved retinal function, as well as reduced TNFalpha and SOCS3-induced insulin resistance in all samples. Salicylates 23-33 tumor necrosis factor Rattus norvegicus 94-102