PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 21859832-8 2011 Several single-nucleotide polymorphisms interacted significant with both NF-kappaB1 and IL6 and with aspirin/non-steroidal anti-inflammatory drugs and cigarette smoking. Aspirin 101-108 interleukin 6 Homo sapiens 88-91 20349206-4 2011 With RKO cells, aspirin reduced IL-6, IL-1ra, and IL-10 synthesis and enhanced IFNgamma secretion, while IL-1beta remained unchanged. Aspirin 16-23 interleukin 6 Homo sapiens 32-36 20158569-8 2011 The standard anti-inflammatory drugs aspirin and indomethacin (Indo) reduced the synergistic IL-6 production by 60%. Aspirin 37-44 interleukin 6 Homo sapiens 93-97 20158569-11 2011 Combination of statins with aspirin and/or Indo resulted in complete inhibition of the synergistic IL-6 production. Aspirin 28-35 interleukin 6 Homo sapiens 99-103 20950383-6 2010 Across the pooled study sample, change in ambulatory activity was significantly correlated with change in interleukin-6 (r = -0.32, P = 0.01) after adjustment for group, age, sex, ethnicity, aspirin and statin medication, baseline body mass index and change in body mass index. Aspirin 191-198 interleukin 6 Homo sapiens 106-119 19942655-5 2010 The addition of acetylsalicylic acid had significantly suppressive effect on the IL-6 production by lipopolysaccharide-stimulated patients" peripheral blood mononuclear cells. Aspirin 16-36 interleukin 6 Homo sapiens 81-85 18034847-8 2008 Aspirin reduced IL-6 with 0.7 +/- 0.5 pg/ml, whereas use of placebo resulted in a mean increase of 0.2 +/- 0.8 pg/ml (P = 0.302). Aspirin 0-7 interleukin 6 Homo sapiens 16-20 19903376-6 2009 KEY FINDINGS: The blood levels of hs-CRP, TNF-alpha, IL-6 and TXB2 were significantly decreased after 2 weeks of treatment with 300 mg/day of aspirin. Aspirin 142-149 interleukin 6 Homo sapiens 53-57 19903376-8 2009 The blood level of IL-6 in the 300 mg/day aspirin group was significantly lower than that in the other two groups after 2 weeks of therapy. Aspirin 42-49 interleukin 6 Homo sapiens 19-23 19595669-0 2009 Aspirin induces apoptosis through the blockade of IL-6-STAT3 signaling pathway in human glioblastoma A172 cells. Aspirin 0-7 interleukin 6 Homo sapiens 50-54 19595669-6 2009 We also showed that the expression and secretion of interleukin-6 (IL-6), leading to STAT3 phosphorylation, was inhibited by aspirin. Aspirin 125-132 interleukin 6 Homo sapiens 52-65 19595669-6 2009 We also showed that the expression and secretion of interleukin-6 (IL-6), leading to STAT3 phosphorylation, was inhibited by aspirin. Aspirin 125-132 interleukin 6 Homo sapiens 67-71 19595669-7 2009 When administered exogenous IL-6 to aspirin-treated A172 cells, the phosphorylation of STAT3 and cellular apoptosis were restrained compared to aspirin only-treated cells. Aspirin 36-43 interleukin 6 Homo sapiens 28-32 19595669-7 2009 When administered exogenous IL-6 to aspirin-treated A172 cells, the phosphorylation of STAT3 and cellular apoptosis were restrained compared to aspirin only-treated cells. Aspirin 144-151 interleukin 6 Homo sapiens 28-32 19595669-8 2009 Taken together, our results indicate that aspirin causes apoptosis via down-regulation of IL-6-dependent STAT3 signaling, suggesting that aspirin could be therapeutically useful for a potential anti-glioblastoma therapeutic approach. Aspirin 42-49 interleukin 6 Homo sapiens 90-94 19595669-8 2009 Taken together, our results indicate that aspirin causes apoptosis via down-regulation of IL-6-dependent STAT3 signaling, suggesting that aspirin could be therapeutically useful for a potential anti-glioblastoma therapeutic approach. Aspirin 138-145 interleukin 6 Homo sapiens 90-94 19641312-4 2009 RESULTS: An increase in IL-6 level was found in the aspirin group when compared to the triflusal group at the third and seventh day (p < 0.05). Aspirin 52-59 interleukin 6 Homo sapiens 24-28 18982014-4 2008 DESIGN: The effect of acetylsalicylic acid (ASA), an inhibitor of COX, on IL-6 was assessed in human subjects and mice. Aspirin 22-42 interleukin 6 Homo sapiens 74-78 18982014-4 2008 DESIGN: The effect of acetylsalicylic acid (ASA), an inhibitor of COX, on IL-6 was assessed in human subjects and mice. Aspirin 44-47 interleukin 6 Homo sapiens 74-78 18982014-6 2008 METHODS AND RESULTS: In obese humans, low-dose ASA (150 mg day(-1) for 10 days) inhibited systemic IL-6 and reduced IL-6 release from SC WAT ex vivo (0.2 mM). Aspirin 47-50 interleukin 6 Homo sapiens 99-103 18982014-6 2008 METHODS AND RESULTS: In obese humans, low-dose ASA (150 mg day(-1) for 10 days) inhibited systemic IL-6 and reduced IL-6 release from SC WAT ex vivo (0.2 mM). Aspirin 47-50 interleukin 6 Homo sapiens 116-120 18992263-7 2009 Most associations varied by recent aspirin/NSAID use: IL6 rs1800796 and rs1800795 polymorphisms were associated inversely with tumor mutations in the presence of aspirin/NSAIDs; POMC significantly reduced risk of Ki-ras-mutated tumors when aspirin/NSAIDs were not used; the TCF7L2 rs7903146 was associated with reduced risk of Ki-ras-mutated tumors in the presence of aspirin and increased risk in the absence of aspirin. Aspirin 35-42 interleukin 6 Homo sapiens 54-57 18992263-7 2009 Most associations varied by recent aspirin/NSAID use: IL6 rs1800796 and rs1800795 polymorphisms were associated inversely with tumor mutations in the presence of aspirin/NSAIDs; POMC significantly reduced risk of Ki-ras-mutated tumors when aspirin/NSAIDs were not used; the TCF7L2 rs7903146 was associated with reduced risk of Ki-ras-mutated tumors in the presence of aspirin and increased risk in the absence of aspirin. Aspirin 162-169 interleukin 6 Homo sapiens 54-57 18992263-7 2009 Most associations varied by recent aspirin/NSAID use: IL6 rs1800796 and rs1800795 polymorphisms were associated inversely with tumor mutations in the presence of aspirin/NSAIDs; POMC significantly reduced risk of Ki-ras-mutated tumors when aspirin/NSAIDs were not used; the TCF7L2 rs7903146 was associated with reduced risk of Ki-ras-mutated tumors in the presence of aspirin and increased risk in the absence of aspirin. Aspirin 162-169 interleukin 6 Homo sapiens 54-57 18992263-7 2009 Most associations varied by recent aspirin/NSAID use: IL6 rs1800796 and rs1800795 polymorphisms were associated inversely with tumor mutations in the presence of aspirin/NSAIDs; POMC significantly reduced risk of Ki-ras-mutated tumors when aspirin/NSAIDs were not used; the TCF7L2 rs7903146 was associated with reduced risk of Ki-ras-mutated tumors in the presence of aspirin and increased risk in the absence of aspirin. Aspirin 162-169 interleukin 6 Homo sapiens 54-57 18992263-7 2009 Most associations varied by recent aspirin/NSAID use: IL6 rs1800796 and rs1800795 polymorphisms were associated inversely with tumor mutations in the presence of aspirin/NSAIDs; POMC significantly reduced risk of Ki-ras-mutated tumors when aspirin/NSAIDs were not used; the TCF7L2 rs7903146 was associated with reduced risk of Ki-ras-mutated tumors in the presence of aspirin and increased risk in the absence of aspirin. Aspirin 162-169 interleukin 6 Homo sapiens 54-57 19641312-9 2009 CONCLUSION: Triflusal modulates additional mechanisms to those of aspirin [pro-inflammatory (IL-6) and chemokine (MIP-1 and MCP-1) pathways] that could participate in the ischemic damage process following human acute stroke. Aspirin 66-73 interleukin 6 Homo sapiens 93-97 18319729-7 2008 The stroke aspirin-resistant group had higher levels of IL-6 than the stroke aspirin-sensitive group (2.4+/-1 versus 1.8+/-0.9 ng/mL, P=0.037). Aspirin 11-18 interleukin 6 Homo sapiens 56-60 18319729-9 2008 These analyses showed that IL-6 was independently associated with stroke severity as the outcome (B=3.738, P=0.036), and aspirin resistance was independently associated with IL-6 (B=0.765, P=0.005) as the outcome. Aspirin 121-128 interleukin 6 Homo sapiens 174-178 17306251-6 2007 We previously demonstrated that treatment of mast cells with heat shock or acetylsalicylic acid results in an increase of TNF-alpha and IL-6 release. Aspirin 75-95 interleukin 6 Homo sapiens 136-140 17881186-0 2008 Aspirin, but not propranolol, attenuates the acute stress-induced increase in circulating levels of interleukin-6: a randomized, double-blind, placebo-controlled study. Aspirin 0-7 interleukin 6 Homo sapiens 100-113 17881186-2 2008 We investigated the effect of aspirin and propranolol on the responsiveness of plasma IL-6 levels to acute psychosocial stress. Aspirin 30-37 interleukin 6 Homo sapiens 86-90 17881186-6 2008 The change in IL-6 from pre-stress to 105 min post-stress differed between subjects with aspirin medication and those without (p =0.033; eta p2=0.059). Aspirin 89-96 interleukin 6 Homo sapiens 14-18 17881186-7 2008 IL-6 levels increased less from pre-stress to 105 min post-stress (p <0.027) and were lower (p =0.010) at 105 min post-stress in subjects with aspirin than in subjects without aspirin. Aspirin 146-153 interleukin 6 Homo sapiens 0-4 17881186-7 2008 IL-6 levels increased less from pre-stress to 105 min post-stress (p <0.027) and were lower (p =0.010) at 105 min post-stress in subjects with aspirin than in subjects without aspirin. Aspirin 179-186 interleukin 6 Homo sapiens 0-4 17881186-11 2008 Aspirin but not propranolol attenuated the stress-induced increase in plasma IL-6 levels. Aspirin 0-7 interleukin 6 Homo sapiens 77-81 17694420-6 2007 Both IL6 polymorphisms were associated with significant interaction with current use of aspirin/NSAIDs to alter risk of colon cancer: individuals with a C allele in either polymorphism who were current users of aspirin/NSAIDs had the lowest colon cancer risk. Aspirin 88-95 interleukin 6 Homo sapiens 5-8 17694420-6 2007 Both IL6 polymorphisms were associated with significant interaction with current use of aspirin/NSAIDs to alter risk of colon cancer: individuals with a C allele in either polymorphism who were current users of aspirin/NSAIDs had the lowest colon cancer risk. Aspirin 211-218 interleukin 6 Homo sapiens 5-8 17694420-7 2007 CRC risk also was associated with an interaction between VDR and IL6 genotypes that was modified by current use of aspirin/NSAIDs. Aspirin 115-122 interleukin 6 Homo sapiens 65-68 17416766-11 2007 IL6 genotype and haplotype significantly modified the association between aspirin and breast cancer, with the greatest effect modification being among women not recently exposed to hormones [P interaction = 0.06 (for non-Hispanic white) and 0.04 (for Hispanic/Native American) and SNP rs1800796 or -572G>C]. Aspirin 74-81 interleukin 6 Homo sapiens 0-3 17416766-12 2007 These data suggest that IL6 is associated with breast cancer risk and modifies the association between estrogen and aspirin and breast cancer risk. Aspirin 116-123 interleukin 6 Homo sapiens 24-27 12117719-6 2002 Attenuation of the C pneumoniae-induced activation of NF-kappaB by aspirin also reduced the secretion of interleukin-6 and interleukin-8, indicating efficient inhibition of NF-kappaB gene expression. Aspirin 67-74 interleukin 6 Homo sapiens 105-118 15763541-4 2005 ASA blocked the expression of cyclooxygenase-2, the production of tumor necrosis factor-alpha and interleukin-6, and the release of granule mediators from mast cells in a concentration-dependent fashion. Aspirin 0-3 interleukin 6 Homo sapiens 98-111 17699316-10 2006 Serum IL-6 concentration decreased with aspirin treatment but not significantly (P = 0.1). Aspirin 40-47 interleukin 6 Homo sapiens 6-10 15136366-8 2004 CONCLUSION: Patients recovering from ACS had lower levels of CRP and IL-6 at 1 month and lower CRP levels at 3 months when treated with rofecoxib plus aspirin. Aspirin 151-158 interleukin 6 Homo sapiens 69-73 14742690-11 2004 Aspirin also enhanced steady-state mRNA levels of other IL-1 modulated genes (IL-1beta, IL-6, groalpha, and TNFalpha) that are likewise regulated at the level of message stability via p38 activation. Aspirin 0-7 interleukin 6 Homo sapiens 88-92 12534448-2 2002 The aim of this study was to explore if prior aspirin therapy in unstable angina (UA) patients could modify systemic inflammatory markers such as interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-alpha) and intercellular adhesion molecule-1 (ICAM-1) and the expression of endothelial nitric oxide synthase (eNOS) in neutrophils. Aspirin 46-53 interleukin 6 Homo sapiens 146-159 12534448-2 2002 The aim of this study was to explore if prior aspirin therapy in unstable angina (UA) patients could modify systemic inflammatory markers such as interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-alpha) and intercellular adhesion molecule-1 (ICAM-1) and the expression of endothelial nitric oxide synthase (eNOS) in neutrophils. Aspirin 46-53 interleukin 6 Homo sapiens 161-165 12534448-7 2002 Plasma levels of both IL-6 and ICAM-1 were reduced in patients taking aspirin. Aspirin 70-77 interleukin 6 Homo sapiens 22-26 1280631-1 1992 The current study was designed to observe the effects of drugs used for the treatment of inflammatory diseases (glucocorticoid, aspirin, and gamma globulin) on interleukin 6 (IL-6) production in the liver which may be involved in acute phase protein stimulation. Aspirin 128-135 interleukin 6 Homo sapiens 175-179 10567380-8 1999 Furthermore, enhanced production, mRNA expression, and gene transcription of apo(a) by interleukin-6 were also inhibited by aspirin. Aspirin 124-131 interleukin 6 Homo sapiens 87-100 10458713-9 1999 MCSF, IL-6, and CRP were all reduced after 6 weeks of aspirin treatment (P<0.05). Aspirin 54-61 interleukin 6 Homo sapiens 6-10 1280631-6 1992 At 48 h after addition of glucocorticoid and aspirin, there was a suppression of IL-6 activity in the culture supernatants, which was associated with a decrease of mRNA level in the cells. Aspirin 45-52 interleukin 6 Homo sapiens 81-85 1280631-8 1992 These data demonstrate that glucocorticoid and aspirin are potent regulators of IL-6 synthesis in the hepatoma cell. Aspirin 47-54 interleukin 6 Homo sapiens 80-84 1814850-4 1991 Aspirin, ibuprofen, and phenylbutazone also inhibited IL-6 production by adherent cells stimulated with lipopolysaccharide (LPS). Aspirin 0-7 interleukin 6 Homo sapiens 54-58 35433995-13 2022 Both doses of ASA + CPG decreased pro-inflammatory cytokine interleukin (IL)-6 expression 21 days after stroke. Aspirin 14-17 interleukin 6 Homo sapiens 60-78 34428217-5 2021 Experiments demonstrate for the first time that plasma concentrations of Acetylsalicylic acid significantly increased TLR ligand-triggered IL-1beta, IL-10, and IL-6 production in a dose-dependent manner. Aspirin 73-93 interleukin 6 Homo sapiens 160-164 35366783-7 2022 In COVID-19 patients, aspirin can reduce CRP, IL-6 levels, and platelet aggregation by inhibiting thromboxane A2. Aspirin 22-29 interleukin 6 Homo sapiens 46-50 35433995-14 2022 Taken together, these results demonstrated that combination treatment with ASA + CPG improved long-term neurological function after stroke and may inhibit platelet-neutrophil interaction by decreasing the concentration of pro-inflammatory cytokine, IL-6. Aspirin 75-78 interleukin 6 Homo sapiens 249-253 33959001-11 2021 In MSCs, atorvastatin and aspirin combination reduced the release of pro-inflammatory cytokines such as IL-6, IL-8, MCP-1 and IFN-gamma. Aspirin 26-33 interleukin 6 Homo sapiens 104-108 32955700-8 2021 Subsequent multivariate logistic regression analysis revealed that among these inflammatory cytokines, only IL-6 (P = 0.019) independently predicted higher ASAS 20 response to celecoxib at W12, and it had a fair value for predicting ASAS 20 response to celecoxib at W12 (area under the curve: 0.666, 95% confidence interval: 0.561-0.771) by receiver-operating characteristic curve analysis. Aspirin 156-160 interleukin 6 Homo sapiens 108-112 33959001-13 2021 Combination of atorvastatin and aspirin had additive effect on reducing the secretion of IL-6 from co-cultures of stroke Mo and MSCs. Aspirin 32-39 interleukin 6 Homo sapiens 89-93 31220426-13 2019 In addition, in co-cultures independent of Mo origin, ASA reduced IL-6, IL-8, MCP-1, and TNF-alpha. Aspirin 54-57 interleukin 6 Homo sapiens 66-70 32071459-12 2020 Real-time PCR showed that 1-100 mumol/L meloxicam or 100 mumol/L aspirin down-regulated significantly the mRNA expression of TNF-alpha and IL-6 of LPS-hDPCs (P<0.05), and 100 mumol/L meloxicam down-regulated IL-6 and TNF-alpha more significantly than 100 mumol/L aspirin of LPS-hDPCs (P<0.05). Aspirin 65-72 interleukin 6 Homo sapiens 211-215 32053214-12 2020 Low concentration (0.05mM) ASA reduced inflammatory cytokines IL-6 (p < 0.001), CCL21 (P < 0.05) and MMP-9 (p < 0.05) in an ex vivo pulpitis model. Aspirin 27-30 interleukin 6 Homo sapiens 62-66 32071459-12 2020 Real-time PCR showed that 1-100 mumol/L meloxicam or 100 mumol/L aspirin down-regulated significantly the mRNA expression of TNF-alpha and IL-6 of LPS-hDPCs (P<0.05), and 100 mumol/L meloxicam down-regulated IL-6 and TNF-alpha more significantly than 100 mumol/L aspirin of LPS-hDPCs (P<0.05). Aspirin 65-72 interleukin 6 Homo sapiens 139-143 26025192-8 2015 CONCLUSIONS: Our data suggest that TNF-alpha and IL-6, but not CRP, are associated with the prevalence and severity of CKD, independent from established CKD risk factors, history of cardiovascular disease, and use of antihypertensive, antidiabetic, and lipid-lowering agents and aspirin. Aspirin 279-286 interleukin 6 Homo sapiens 49-53 31092431-8 2019 CONCLUSION: Plasmatic doses of ASA and celecoxib altered the expression of IL6 and the gene expression of chemokines (ligands and receptors) and cytokines in a dose- and time-dependent manner. Aspirin 31-34 interleukin 6 Homo sapiens 75-78 31010006-5 2019 Based on alterations in morphology, modulation of capillary formation, and changes in endothelial and mesenchymal marker profile, our findings demonstrate that higher levels of tumor growth factor-betas and interleukin-6 enhance cancer-associated fibroblast-like cell formation through endothelial-mesenchymal transition and that nonsteroidal anti-inflammatory drug treatment (aspirin and ibuprofen) is able to inhibit this phenomenon. Aspirin 377-384 interleukin 6 Homo sapiens 207-220 30585832-9 2019 In contrast, acetylsalicylic acid treatment resulted in enhanced plasma levels of tumor necrosis factor-alpha (+53%; p = 0.02), interleukin-6 (+91%; p = 0.03), and interleukin-8 (+42%; p = 0.02) upon the second challenge, whereas plasma levels of the key antiinflammatory cytokine interleukin-10 were attenuated (-40%; p = 0.003). Aspirin 13-33 interleukin 6 Homo sapiens 128-141 29568915-8 2018 Furthermore, it was confirmed that the signaling pathways involving CX3CL1-NF-kappaB, IL-6 and TNF-alpha were partly inhibited by aspirin. Aspirin 130-137 interleukin 6 Homo sapiens 86-90 26774572-7 2016 Interestingly, ASP- and PROP-containing substrates not only showed reduced adhesion of platelets and delayed coagulation time, but also drastically reduced the expression level of IL-8 and IL-6. Aspirin 15-18 interleukin 6 Homo sapiens 189-193 28899503-16 2017 Secretion of IL-8 and IL-6 was reduced by STW1 and ASA. Aspirin 51-54 interleukin 6 Homo sapiens 22-26 26615369-9 2016 Aspirin challenge induced the release of uLTE4, IL-6 and increased the number of CD4(+)CD45RA(-)CD45RO(+) memory T-cells only in AERD patients but failed to reduce the levels of sCD40L as observed in non-AERD subjects. Aspirin 0-7 interleukin 6 Homo sapiens 48-52 26615369-10 2016 Further, IL-8 and sIL-5R-alpha levels directly correlated with the PD20ASA and the effects of aspirin on IL-6 and number of memory T-cells was more pronounced in subjects showing more strong reaction (bronchial and nasal). Aspirin 94-101 interleukin 6 Homo sapiens 105-109 26615369-12 2016 Systemic response to oral aspirin challenge was related to an increase in serum IL-6 and the number of circulating memory T-cells in AERD patients. Aspirin 26-33 interleukin 6 Homo sapiens 80-84 24880897-9 2014 However, treatment of inflammatory M1 macrophages with aspirin reduced secretion of the pro-inflammatory cytokines IL-1beta and IL-6, and increased secretion of the anti-inflammatory IL-10. Aspirin 55-62 interleukin 6 Homo sapiens 128-132 24649055-10 2013 The application of aspirin (0.1 mM) significantly inhibited the activation of ERK1/2 and NF-kappaB, the expression of TNF-alpha, IL-6, IL-1beta and MCP-1 genes and the secretion of TNF-alpha and IL-6. Aspirin 19-26 interleukin 6 Homo sapiens 129-133 24649055-10 2013 The application of aspirin (0.1 mM) significantly inhibited the activation of ERK1/2 and NF-kappaB, the expression of TNF-alpha, IL-6, IL-1beta and MCP-1 genes and the secretion of TNF-alpha and IL-6. Aspirin 19-26 interleukin 6 Homo sapiens 195-199 23398903-14 2013 Combination of Aspirin and Docosahexaenoic Acid showed augmentation in total Glutathione production during TLR-7 stimulation as well as a reduction in IL-6, TNF-alpha and Nitric Oxide. Aspirin 15-22 interleukin 6 Homo sapiens 151-155 24469880-8 2013 CONCLUSIONS: Increasing the dose of ASA from 75 mg to 150 mg daily or switching ASA 75 mg to clopidogrel 75 mg daily may reduce concentrations of some inflammatory markers (in particular hsCRP, IL-6 and CD40L) in T2DM patients with HPR treated previously with 75 mg of ASA. Aspirin 36-39 interleukin 6 Homo sapiens 194-198 24469880-8 2013 CONCLUSIONS: Increasing the dose of ASA from 75 mg to 150 mg daily or switching ASA 75 mg to clopidogrel 75 mg daily may reduce concentrations of some inflammatory markers (in particular hsCRP, IL-6 and CD40L) in T2DM patients with HPR treated previously with 75 mg of ASA. Aspirin 80-83 interleukin 6 Homo sapiens 194-198 24469880-8 2013 CONCLUSIONS: Increasing the dose of ASA from 75 mg to 150 mg daily or switching ASA 75 mg to clopidogrel 75 mg daily may reduce concentrations of some inflammatory markers (in particular hsCRP, IL-6 and CD40L) in T2DM patients with HPR treated previously with 75 mg of ASA. Aspirin 80-83 interleukin 6 Homo sapiens 194-198 23506529-3 2013 Aspirin is a non-steroidal anti-inflammatory drug that is an irreversible inhibitor of both cyclooxygenase (COX)-1 and COX-2, It stimulates endogenous production of anti-inflammatory regulatory "braking signals", including lipoxins, which dampen the inflammatory response and reduce levels of inflammatory biomarkers, including C-reactive protein, tumor necrosis factor-alpha and interleukin (IL)--6, but not negative immunoregulatory cytokines, such as IL-4 and IL-10. Aspirin 0-7 interleukin 6 Homo sapiens 380-399