PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 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 C-C motif chemokine ligand 2 Homo sapiens 116-121 24315932-8 2014 We found that ritonavir administration caused intestinal damage and its co-administration with naproxen or ASA exacerbated the severity of injury and intestinal inflammation, as assessed by measuring haematocrit, MPO, mucosal levels of PGE2 and mRNA levels of iNOS, MCP-1 and VLA-1. Aspirin 107-110 C-C motif chemokine ligand 2 Homo sapiens 266-271 30392338-0 2018 [Aspirin inhibits cell stemness of esophageal cancer by downregulation of chemokine CCL2]. Aspirin 1-8 C-C motif chemokine ligand 2 Homo sapiens 84-88 30392338-8 2018 When chemokine CCL2 was knocked down, the levels of Nanog gene in M2+ shCCL2-KYSE450+ ASA group and M2+ shCCL2-KYSE450 group were decreased to 1.22+-0.11 and 1.17+-0.08, respectively, and there was no statistically significant difference between them (P=0.69). Aspirin 86-89 C-C motif chemokine ligand 2 Homo sapiens 15-19 30392338-11 2018 Conclusions: Tumor-associated macrophages enhances the stemness of esophageal cancer cells, whereas aspirin attenuates the stemness by suppressing the expression of CCL2. Aspirin 100-107 C-C motif chemokine ligand 2 Homo sapiens 165-169 26492523-11 2016 Aspirin, U0126, LY294002 and 5z-7-oxozeaenol attenuated the IL-1beta-induced MCP-1 expression. Aspirin 0-7 C-C motif chemokine ligand 2 Homo sapiens 77-82 26085050-2 2015 In ACS, aspirin at antiplatelet doses exhibits anti-inflammatory effects as seen from the decrease in inflammation markers such as CRP, M-CSF, MCP-1 and others. Aspirin 8-15 C-C motif chemokine ligand 2 Homo sapiens 143-148 26294325-5 2015 Of the top 10 genes (fold-change > 10, P < 10(-10)) regulated by metformin plus aspirin, PCDH18, CCL2, RASL11A, FAM111B and BMP5 were down-regulated >= 20-fold, while NGFR, NPTX1, C7orf57, MRPL23AS1 and UNC5B were up-regulated >= 10-fold. Aspirin 86-93 C-C motif chemokine ligand 2 Homo sapiens 103-107 31220426-11 2019 RESULTS: Overall Mo from control subjects exposed to ASA showed increased secretion of IL-1RA, IL-8, MCP-1, and TNF-alpha and Mo from stroke patients showed greater release of IL-1RA and MCP-1. Aspirin 53-56 C-C motif chemokine ligand 2 Homo sapiens 101-106 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 C-C motif chemokine ligand 2 Homo sapiens 78-83 22561694-6 2012 In addition, the increased transcription of MCP-1 was detectable at later maturation phase of adipogenesis, which was prevented by co-incubation with aspirin. Aspirin 150-157 C-C motif chemokine ligand 2 Homo sapiens 44-49 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 C-C motif chemokine ligand 2 Homo sapiens 148-153 22561694-7 2012 Although 15d-PGJ(2) was more potent than Delta(12)-PGJ(2), both PGJ(2) derivatives series had similar effects to rescue dose-dependently the expression of the MCP-1 gene attenuated by aspirin. Aspirin 184-191 C-C motif chemokine ligand 2 Homo sapiens 159-164 16600694-5 2006 The results showed that (i) aspirin, fenofibrate and clofibrate decrease significantly the MCP-1 expression and secretion in human endothelial cells; (ii) the high glucose up-regulated expression of MCP-1 in endothelial cells was significantly reduced by inhibitors of NF-kB and reactive oxygen species; (iii) all drugs notably decrease the level of the reactive oxygen species and activation of NF-kB and AP-1. Aspirin 28-35 C-C motif chemokine ligand 2 Homo sapiens 91-96 22942727-2 2012 Preclinical studies indicate that treatment with acetylsalicylic acid + extended-release dipyridamole (ASA + ER-DP) has anti-inflammatory and thereby neuroprotective effects by inhibition of monocyte chemotactic protein-1 (MCP-1) expression. Aspirin 49-69 C-C motif chemokine ligand 2 Homo sapiens 191-221 22942727-2 2012 Preclinical studies indicate that treatment with acetylsalicylic acid + extended-release dipyridamole (ASA + ER-DP) has anti-inflammatory and thereby neuroprotective effects by inhibition of monocyte chemotactic protein-1 (MCP-1) expression. Aspirin 49-69 C-C motif chemokine ligand 2 Homo sapiens 223-228 22942727-2 2012 Preclinical studies indicate that treatment with acetylsalicylic acid + extended-release dipyridamole (ASA + ER-DP) has anti-inflammatory and thereby neuroprotective effects by inhibition of monocyte chemotactic protein-1 (MCP-1) expression. Aspirin 103-106 C-C motif chemokine ligand 2 Homo sapiens 191-221 22942727-2 2012 Preclinical studies indicate that treatment with acetylsalicylic acid + extended-release dipyridamole (ASA + ER-DP) has anti-inflammatory and thereby neuroprotective effects by inhibition of monocyte chemotactic protein-1 (MCP-1) expression. Aspirin 103-106 C-C motif chemokine ligand 2 Homo sapiens 223-228 22942727-3 2012 We hypothesized that early treatment with ASA + ER-DP will reduce levels of MCP-1 also in patients with ischemic stroke. Aspirin 42-45 C-C motif chemokine ligand 2 Homo sapiens 76-81 22942727-8 2012 Comparisons within MCP-1 baseline quartiles indicated that patients in the highest quartile (>217-973 pg/mL) showed improved outcome at 90 days if treated with ASA + ER-DP in comparison to treatment with ASA alone (p = 0.004). Aspirin 163-166 C-C motif chemokine ligand 2 Homo sapiens 19-24 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 C-C motif chemokine ligand 2 Homo sapiens 124-129 17296320-1 2007 OBJECTIVES: Platelet monocyte aggregates (PMA) and monocyte chemoattractant protein-1 (MCP-1) play a significant role in atherosclerotic disease but the effect of aspirin and their role in peripheral arterial disease (PAD) requires further investigation. Aspirin 163-170 C-C motif chemokine ligand 2 Homo sapiens 87-92 17080224-7 2006 In the aspirin group we found significantly lower levels of TNFa and MCP-1 after one year; 1.00 versus 1.16 pg/ml (p < 0.001) and 245 versus 261 pg/ml (p < 0.001), respectively. Aspirin 7-14 C-C motif chemokine ligand 2 Homo sapiens 69-74 16600694-0 2006 Aspirin and PPAR-alpha activators inhibit monocyte chemoattractant protein-1 expression induced by high glucose concentration in human endothelial cells. Aspirin 0-7 C-C motif chemokine ligand 2 Homo sapiens 42-76 20819511-6 2010 Activation of p38 mitogen activated protein kinase and NF-kappaB, the expression of intercellular adhesion molecule-1 and monocyte chemotactic protein-1, which were only mildly affected by aspirin or pravastatin alone, were significantly attenuated by their combination. Aspirin 189-196 C-C motif chemokine ligand 2 Homo sapiens 122-152 16600694-6 2006 Together, the findings indicate that in endothelial cells aspirin and PPAR-alpha activators reduce the high glucose-increased expression of MCP-1 by a mechanism that includes the inhibition of reactive oxygen species, and decrease of AP-1 and NF-kB activation. Aspirin 58-65 C-C motif chemokine ligand 2 Homo sapiens 140-145 15136050-0 2004 Aspirin inhibits monocyte chemoattractant protein-1 and interleukin-8 expression in TNF-alpha stimulated human umbilical vein endothelial cells. Aspirin 0-7 C-C motif chemokine ligand 2 Homo sapiens 17-51 15136050-6 2004 In this study, we found that aspirin inhibited TNF-alpha (10 ng/ml)-induced MCP-1 and IL-8 expression at the RNA and protein levels in human umbilical vein endothelial cells (HUVECs), monocyte adhesion and transmigration, and that its inhibitory effects were not due to decreased HUVEC viability as assessed by MTT test. Aspirin 29-36 C-C motif chemokine ligand 2 Homo sapiens 76-81 15136050-7 2004 Aspirin at the dose as low as 10 microg/ml significantly inhibited the release of TNF-stimulated MCP-1 by 29.1% (P = 0.008) and IL-8 by 26.9% (P = 0.0146) as compared to TNF-stimulated release. Aspirin 0-7 C-C motif chemokine ligand 2 Homo sapiens 97-102 15136050-11 2004 These results in our study suggest that aspirin inhibits TNF-alpha stimulated MCP-1 and IL-8 release in HUVECs, for its additional therapeutic effects of aspirin in causing atherosclerosis. Aspirin 40-47 C-C motif chemokine ligand 2 Homo sapiens 78-83