PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 30959503-10 2019 Also, secretion of the studied solutes, with the exception of ICAM-1, was reduced in the presence of NAC: IL6 -34%, p < 0.01; VEGF -40%, p < 0.005; vWF -25%, p < 0.001; t-PA -47%, p < 0.01, and MMP9 -37%, p < 0.001. Acetylcysteine 101-104 interleukin 6 Homo sapiens 106-109 34208683-5 2021 As an anti-inflammatory compound, NAC can reduce levels of tumor necrosis factor-alpha (TNF-alpha) and interleukins (IL-6 and IL-1beta) by suppressing the activity of nuclear factor kappa B (NF-kappaB). Acetylcysteine 34-37 interleukin 6 Homo sapiens 117-121 33404763-12 2021 Ten-minute NAC treatment downregulated the IL-6 and TNF-alpha expression, whereas the expression of Bcl-2/Bax and Mfn-2/Drp-1 ratios was upregulated at 6 h. CONCLUSIONS: Under the LPS-induced inflammatory condition, NAC stimulated APC survival and decreased inflammation. Acetylcysteine 11-14 interleukin 6 Homo sapiens 43-47 33503268-12 2021 NAC supplementation to the MTA extract significantly reduced the level of IL-6 and TNF-alpha expression (P<0.05). Acetylcysteine 0-3 interleukin 6 Homo sapiens 74-78 33371832-7 2021 Furthermore, NAC decreases TNF-alpha, IL-1beta, IL-6, IL-8, IL-10, and IL-17 serum levels in patients with sepsis, severe burns, acute liver failure, or peritoneal dialysis and may also reduce cytokine storm in COVID-19. Acetylcysteine 13-16 interleukin 6 Homo sapiens 48-52 33146789-10 2021 In addition, using the ROS inhibitor N-acetyl-L-cysteine (NAC), we observed abrogated mRNA expression of several ARPs and production of inflammatory cytokines/chemokines (IL-6, IL-8, MCP-1, and CCL-5) in the CSE-challenged cells suggesting an important role of ROS in regulating CSE-induced autophagy. Acetylcysteine 37-56 interleukin 6 Homo sapiens 171-175 33146789-10 2021 In addition, using the ROS inhibitor N-acetyl-L-cysteine (NAC), we observed abrogated mRNA expression of several ARPs and production of inflammatory cytokines/chemokines (IL-6, IL-8, MCP-1, and CCL-5) in the CSE-challenged cells suggesting an important role of ROS in regulating CSE-induced autophagy. Acetylcysteine 58-61 interleukin 6 Homo sapiens 171-175 32868342-8 2020 In addition, compared to SS2-infected STEC, PCV2/SS2 coinfection and pretreatment of STEC with NAC prior to SS2 infection both down-regulated the expression of inflammatory cytokines IL-6, TNF-alpha and IL-1beta. Acetylcysteine 95-98 interleukin 6 Homo sapiens 183-187 32361974-5 2020 The presence of NAC antagonized the ROS production, expressions of IRE1alpha and p-IRE1alpha; however, STF-083010 could decrease the expression levels of GRP78, XBP1, NF-kappaB, and p-NF-kappaB and attenuate IL-1beta, IL-6, TNF-alpha, VCAM-1, and ET-1 release induced by endosulfan. Acetylcysteine 16-19 interleukin 6 Homo sapiens 218-222 30520466-4 2019 First, N-acetyl-l-cysteine was used to decrease the viscosity of HSF samples and consequently enhance bacterial isolation with vancomycin-coated nano-magnetic beads. Acetylcysteine 7-26 interleukin 6 Homo sapiens 65-68 30255760-6 2019 RESULTS: Results showed that in the NAC group, the serum levels of MDA, NO, IL-6, TNF-alpha, ESR and CRP were significantly lower than the baseline. Acetylcysteine 36-39 interleukin 6 Homo sapiens 76-80 34936178-9 2021 CONCLUSION: The RCTs examined suggest that prophylactic administration of corticosteroid agents and NAC can reduce the severity of pancreatitis as indicated by histopathologic markers, serum amylase and IL-6 levels. Acetylcysteine 100-103 interleukin 6 Homo sapiens 203-207 32799012-9 2020 Oral supplementation of NAC reduced serum level of C-reactive protein (CRP) [WMD: -0.61 mg/L, 95% CI: -1.18 to -0.03, P = 0.039, I2 = 79.6%], and interleukin-6 (IL-6) [WMD: -0.43 pg/mL, 95% CI: -0.69 to -0.17, P = 0.001, I2 = 89.3%]. Acetylcysteine 24-27 interleukin 6 Homo sapiens 146-159 32799012-9 2020 Oral supplementation of NAC reduced serum level of C-reactive protein (CRP) [WMD: -0.61 mg/L, 95% CI: -1.18 to -0.03, P = 0.039, I2 = 79.6%], and interleukin-6 (IL-6) [WMD: -0.43 pg/mL, 95% CI: -0.69 to -0.17, P = 0.001, I2 = 89.3%]. Acetylcysteine 24-27 interleukin 6 Homo sapiens 161-165 32799012-12 2020 CONCLUSION: Oral NAC supplementation reduced serum level of CRP and IL-6, but did not affect other inflammatory biomarkers. Acetylcysteine 17-20 interleukin 6 Homo sapiens 68-72 32726657-13 2020 However, NAC effects were significant in ameliorating TNF-alpha and IL-6 using sensitivity analysis. Acetylcysteine 9-12 interleukin 6 Homo sapiens 68-72 32726657-15 2020 The effects of NAC on amending TNF-alpha and IL-6 levels were significant after sensitivity analysis. Acetylcysteine 15-18 interleukin 6 Homo sapiens 45-49 32551386-6 2020 NAC-related increase in glutathione was associated with significant alterations in tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-6, IL-8 and IL-10 levels secreted in the culture medium. Acetylcysteine 0-3 interleukin 6 Homo sapiens 124-142 32551386-7 2020 A substantial decrease in the IL-6, IL-8 and TNF-alpha levels in the culture medium supplemented with NAC was obvious in hepatocytes recovered 14 days after differentiation. Acetylcysteine 102-105 interleukin 6 Homo sapiens 30-34 31332969-6 2019 The ROS inhibitor N-acetylcysteine and MAPK inhibitors significantly reduced the expression of IL-6 and IL-24 induced by T. forsythia. Acetylcysteine 18-34 interleukin 6 Homo sapiens 95-99 30861304-5 2019 Pre-treatment with the ROS inhibitors N-acetyl cysteine (NAC) and diphenyleneiodonium (DPI) partially attenuated CXCL8 and IL-6 responses to 200 microg/mL, but not to 100 microg/mL Si50. Acetylcysteine 38-55 interleukin 6 Homo sapiens 123-127 30861304-5 2019 Pre-treatment with the ROS inhibitors N-acetyl cysteine (NAC) and diphenyleneiodonium (DPI) partially attenuated CXCL8 and IL-6 responses to 200 microg/mL, but not to 100 microg/mL Si50. Acetylcysteine 57-60 interleukin 6 Homo sapiens 123-127 30317657-5 2019 Furthermore, the antioxidant compound N-acetyl-cysteine eliminated the nicotine-activated production of reactive oxygen species (ROS) and inhibited signal transducer and activator of transcription 3 (STAT-3) phosphorylation; these two mechanisms mediated the upregulation of IL-6 expression by nicotine. Acetylcysteine 38-55 interleukin 6 Homo sapiens 275-279 29113965-9 2018 Furthermore, treatment of atherosclerotic-MSCs with the reactive oxygen species scavenger N-acetyl-l-cysteine reduced the levels of interleukin-6, interleukin-8/C-X-C motif chemokine ligand 8, and monocyte chemoattractant protein-1/chemokine ligand 2 in the MSC secretome and improved MSCs immunosuppressive capacity (P=0.03). Acetylcysteine 90-109 interleukin 6 Homo sapiens 132-145 30571738-8 2018 Finally, anti-Sm mAb still up-regulated the IL-6 production of monocytes in the presence of anti-RNP mAb under the influence of N-acetyl cysteine or pyrrolidine dithiocarbamate that totally abrogated the IL-6 production provoked by anti-Sm mAb alone in the absence of anti-RNP mAb. Acetylcysteine 128-145 interleukin 6 Homo sapiens 44-48 30571738-8 2018 Finally, anti-Sm mAb still up-regulated the IL-6 production of monocytes in the presence of anti-RNP mAb under the influence of N-acetyl cysteine or pyrrolidine dithiocarbamate that totally abrogated the IL-6 production provoked by anti-Sm mAb alone in the absence of anti-RNP mAb. Acetylcysteine 128-145 interleukin 6 Homo sapiens 204-208 29573703-4 2018 The aim of this work was to study the extent of the protective effect of the antioxidant N-acetylcysteine (NAC) over the proinflammatory state (IL-6 and IL-8), oxidative stress (reactive oxygen species, ROS), and CFTR levels, caused by Cigarette Smoke Extract (CSE) in Calu-3 airway epithelial cells. Acetylcysteine 89-105 interleukin 6 Homo sapiens 144-148 29573703-4 2018 The aim of this work was to study the extent of the protective effect of the antioxidant N-acetylcysteine (NAC) over the proinflammatory state (IL-6 and IL-8), oxidative stress (reactive oxygen species, ROS), and CFTR levels, caused by Cigarette Smoke Extract (CSE) in Calu-3 airway epithelial cells. Acetylcysteine 107-110 interleukin 6 Homo sapiens 144-148 28600879-10 2018 After N-acetyl cysteine treatment ROS level was partly abolished providing additional enhancement of IL-6 and suppression of IL-8 and VEGF production. Acetylcysteine 6-23 interleukin 6 Homo sapiens 101-105 29364751-6 2018 Furthermore, HG could promote the generation of reactive oxygen species (ROS), while N-acetyl cysteine, a ROS scavenger, had an inhibitory effect on the expression of TNF-alpha, IL-6 and PAI-1 in HG-treated cells. Acetylcysteine 85-102 interleukin 6 Homo sapiens 178-182 29635121-6 2018 KEY FINDINGS: NAC at high concentrations normalized the peroxidase activity, H2O2, malondialdehyde (MDA), nitric oxide, glutathione (GSH), total antioxidant capacity (TAC), and interleukin 6 (IL-6) (overall change 34.32% +- 4.22%, P < 0.05 vs. LPS-treated). Acetylcysteine 14-17 interleukin 6 Homo sapiens 177-190 29635121-6 2018 KEY FINDINGS: NAC at high concentrations normalized the peroxidase activity, H2O2, malondialdehyde (MDA), nitric oxide, glutathione (GSH), total antioxidant capacity (TAC), and interleukin 6 (IL-6) (overall change 34.32% +- 4.22%, P < 0.05 vs. LPS-treated). Acetylcysteine 14-17 interleukin 6 Homo sapiens 192-196 29635121-7 2018 NAC at low concentrations modulated peroxidase activity, H2O2, MDA, GSH, TAC, and IL-6 (overall change 34.88% +- 7.39%, P < 0.05 vs. LPS-treated). Acetylcysteine 0-3 interleukin 6 Homo sapiens 82-86 29635121-8 2018 NAC at very-low concentrations was effective on peroxidase activity, H2O2, GSH, and IL-6 (overall change 35.05 +- 7.71%, P < 0.05 vs. LPS-treated). Acetylcysteine 0-3 interleukin 6 Homo sapiens 84-88 29635121-9 2018 Binary logistic regression analysis indicated that the modulatory effect of NAC on NKA levels was associated with a reduction of pro-oxidant factors and IL-6, and selectively blocking the NK2 receptor abolished such an association. Acetylcysteine 76-79 interleukin 6 Homo sapiens 153-157 29635121-10 2018 SIGNIFICANCE: This study demonstrates that, along with its well-known antioxidant activity, the protective effect of NAC against the detrimental effect of LPS is due to the modulation of NKA and IL-6 levels. Acetylcysteine 117-120 interleukin 6 Homo sapiens 195-199 27917510-9 2017 N-acetyl-l-cysteine suppressed MeHg-induced activation of IL-6 and IL-8 mRNA expression in U937 macrophages, indicating the effectiveness of N-acetyl-l-cysteine as a therapeutic drug in MeHg-induced inflammation. Acetylcysteine 0-19 interleukin 6 Homo sapiens 58-62 28946937-6 2017 The ROS scavenger N-acetylcysteine inhibited CLB2.0-induced IL-6 secretion, thereby decreasing the CLB2.0-induced MUC5AC expression, whereas CLB2.0-induced MUC1 expression increased. Acetylcysteine 18-34 interleukin 6 Homo sapiens 60-64 27917510-9 2017 N-acetyl-l-cysteine suppressed MeHg-induced activation of IL-6 and IL-8 mRNA expression in U937 macrophages, indicating the effectiveness of N-acetyl-l-cysteine as a therapeutic drug in MeHg-induced inflammation. Acetylcysteine 141-160 interleukin 6 Homo sapiens 58-62 24164541-4 2014 HN2-induced EGFR phosphorylation and IL-6 secretion in NHBECs were inhibited by the antioxidant N-acetyl-L-cysteine (NAC) and by the flavoprotein inhibitor diphenyleneiodonium chloride (DPI). Acetylcysteine 96-115 interleukin 6 Homo sapiens 37-41 26305534-7 2015 The addition of NAC markedly reduced the high glucose-induced ROS activation, Annexin-PI-positive cells, and levels of cleaved caspase-3, BAX, IL-6, and TNF-alpha. Acetylcysteine 16-19 interleukin 6 Homo sapiens 143-147 26006043-0 2015 Suppression of methylmercury-induced IL-6 and MCP-1 expressions by N-acetylcysteine in U-87MG human astrocytoma cells. Acetylcysteine 67-83 interleukin 6 Homo sapiens 37-41 26006043-7 2015 MeHg-induced expression of MCP-1 and IL-6 mRNA was reduced by 10-20% in the presence of 5mM NAC (co-treatment experiment) compared to cells treated with MeHg only. Acetylcysteine 92-95 interleukin 6 Homo sapiens 37-41 26006043-8 2015 Pre-treatment of cells with 0.5 or 5mM NAC at 0.5 or 1h and its subsequent washout before MeHg addition suppressed MCP-1 and IL-6 cytokine expressions. Acetylcysteine 39-42 interleukin 6 Homo sapiens 125-129 28118826-8 2017 Concentrations of NAC >=300 muM inhibited the inflammatory response (release of IL-1beta, IL-8, and TNF-alpha) of human airways induced by the overnight stimulation with LPS, whereas lower concentrations of NAC (>=1 muM) were sufficient to reduce the release of IL-6 elicited by LPS. Acetylcysteine 18-21 interleukin 6 Homo sapiens 268-272 27639126-10 2016 ROS scavenger N-acetylcysteine (NAC) and NF-kappaB inhibitor PDTC showed similar effect on PA-induced secretion of TNF-alpha, IL-6, and expression of ICAM-1. Acetylcysteine 14-30 interleukin 6 Homo sapiens 126-130 27639126-10 2016 ROS scavenger N-acetylcysteine (NAC) and NF-kappaB inhibitor PDTC showed similar effect on PA-induced secretion of TNF-alpha, IL-6, and expression of ICAM-1. Acetylcysteine 32-35 interleukin 6 Homo sapiens 126-130 25058850-6 2015 MDP (an NLRC2 agonist), NAC and AZM, but not Tri-DAP (an NLRC1 agonist), increased IL-6 production in CF cells, indicating that in CF cells IL-6 upregulation is independent of NLRC1, but involves the activation of NLRC2. Acetylcysteine 24-27 interleukin 6 Homo sapiens 83-87 25058850-6 2015 MDP (an NLRC2 agonist), NAC and AZM, but not Tri-DAP (an NLRC1 agonist), increased IL-6 production in CF cells, indicating that in CF cells IL-6 upregulation is independent of NLRC1, but involves the activation of NLRC2. Acetylcysteine 24-27 interleukin 6 Homo sapiens 140-144 25961745-8 2015 3-MA, NAC and DPI inhibited HG-induced interleukin-6 production in BMSCs. Acetylcysteine 6-9 interleukin 6 Homo sapiens 39-52 24681574-14 2014 IL-6 and HSP-70 release was significantly induced by IFN-gamma treatment, which was largely inhibited by NAC. Acetylcysteine 105-108 interleukin 6 Homo sapiens 0-4 22985912-6 2013 N-acetylcysteine prevented morphologic and oxidative derangements, and significantly reduced proinflammatory product secretion (P range<0.0001 to<0.00001 for TNFalpha, VCAM-1, MCP-1, and IL-6); rosuvastatin inhibited morphology and oxidative modifications only. Acetylcysteine 0-16 interleukin 6 Homo sapiens 193-197 24434384-0 2014 The effect of treatment with N-acetylcysteine on the serum levels of C-reactive protein and interleukin-6 in patients on hemodialysis. Acetylcysteine 29-45 interleukin 6 Homo sapiens 92-105 24434384-3 2014 We aimed to assess the effect of three months treatment with oral NAC on the plasma levels of inflammatory mediators like interleukin-6 (IL-6) and C-reactive protein (hs-CRP) in patients on hemodialysis (HD). Acetylcysteine 66-69 interleukin 6 Homo sapiens 122-135 24434384-3 2014 We aimed to assess the effect of three months treatment with oral NAC on the plasma levels of inflammatory mediators like interleukin-6 (IL-6) and C-reactive protein (hs-CRP) in patients on hemodialysis (HD). Acetylcysteine 66-69 interleukin 6 Homo sapiens 137-141 24434384-10 2014 In three subjects who were less than 40 years old, the hs-CRP and IL-6 levels showed an increase following NAC treatment. Acetylcysteine 107-110 interleukin 6 Homo sapiens 66-70 24434384-11 2014 Our study found that short-term oral NAC treatment might result in the reduction of IL-6 and hs-CRP in patients who are on regular HD. Acetylcysteine 37-40 interleukin 6 Homo sapiens 84-88 23434081-8 2013 The levels of inflammatory cytokines (TNF-alpha, IL-1beta, IL-6, and IL-10) in piglet plasma of the NAC group (mixed feeding concentration of 1200 mg/kg) were significantly lower at 3h after LPS stimulation (P<0.05). Acetylcysteine 100-103 interleukin 6 Homo sapiens 59-63 22745145-9 2012 CONCLUSION: short-term oral NAC treatment resulted in reduction of circulating PCT, IL-6, IL-1, C3, sICAM, hsCRP, and TNF- in CAPD patients. Acetylcysteine 28-31 interleukin 6 Homo sapiens 84-88 23351387-2 2012 OBJECTIVE: To evaluate the role of prophylactic ibuprofen and N-acetylcysteine (NAC) on the levels of tumor necrosis factor alpha (TNF- alpha), interleukin- 6(IL-6) and IL-17 and post-treatment pain level in chronic periapical lesions. Acetylcysteine 80-83 interleukin 6 Homo sapiens 144-158 22471522-5 2012 IL-6 combined with IR or Dex increased early intracellular pro-oxidant levels that were causally related to activation of NF-kappaB (nuclear factor kappaB) as determined by the ability of N-acetylcysteine to suppress both pro-oxidant levels and NF-kappaB activation. Acetylcysteine 188-204 interleukin 6 Homo sapiens 0-4 22041018-11 2012 This increase in VEGF and IL6 was blocked by the ROS scavenger N-acetyl cysteine (NAC). Acetylcysteine 63-80 interleukin 6 Homo sapiens 26-29 22041018-11 2012 This increase in VEGF and IL6 was blocked by the ROS scavenger N-acetyl cysteine (NAC). Acetylcysteine 82-85 interleukin 6 Homo sapiens 26-29 21978796-8 2012 Plasma IL-6 was lower on days 4-5 (p<0.05), IL-8 on days 4-6 (p<0.05) and IL-10 on days 4-6 (p<0.05) in NAC group. Acetylcysteine 113-116 interleukin 6 Homo sapiens 7-11 22392142-7 2012 On the other hand, N-acetyl-L-cysteine decreased mRNA stability of ICAM-1 and IL-6 in LPS-treated cells and IL-6 and ICAM-1 in TNF-alpha-treated cells. Acetylcysteine 19-38 interleukin 6 Homo sapiens 78-82 22392142-7 2012 On the other hand, N-acetyl-L-cysteine decreased mRNA stability of ICAM-1 and IL-6 in LPS-treated cells and IL-6 and ICAM-1 in TNF-alpha-treated cells. Acetylcysteine 19-38 interleukin 6 Homo sapiens 108-112 21424515-7 2011 RESULTS: NAC inhibits the inflammatory cytokines TNFalpha, IL-1beta and IL-6 in LPS-activated macrophages under mild oxidative conditions. Acetylcysteine 9-12 interleukin 6 Homo sapiens 72-76 20190028-11 2010 CONCLUSION: Short-term oral NAC treatment resulted in reduction of circulating IL-6, suggesting that such treatment could be a useful strategy in blunting the inflammatory response in PD patients. Acetylcysteine 28-31 interleukin 6 Homo sapiens 79-83 21540553-6 2011 N-acetyl-cysteine (NAC), an antioxidant that restores intracellular glutathione (GSH) concentrations, prevented the IL-6-induced inhibitory effect on D1- and D2-mediated T3 production, which suggests that IL-6 might function by depleting an intracellular thiol cofactor, perhaps GSH. Acetylcysteine 0-17 interleukin 6 Homo sapiens 116-120 21540553-6 2011 N-acetyl-cysteine (NAC), an antioxidant that restores intracellular glutathione (GSH) concentrations, prevented the IL-6-induced inhibitory effect on D1- and D2-mediated T3 production, which suggests that IL-6 might function by depleting an intracellular thiol cofactor, perhaps GSH. Acetylcysteine 0-17 interleukin 6 Homo sapiens 205-209 21540553-6 2011 N-acetyl-cysteine (NAC), an antioxidant that restores intracellular glutathione (GSH) concentrations, prevented the IL-6-induced inhibitory effect on D1- and D2-mediated T3 production, which suggests that IL-6 might function by depleting an intracellular thiol cofactor, perhaps GSH. Acetylcysteine 19-22 interleukin 6 Homo sapiens 116-120 21540553-6 2011 N-acetyl-cysteine (NAC), an antioxidant that restores intracellular glutathione (GSH) concentrations, prevented the IL-6-induced inhibitory effect on D1- and D2-mediated T3 production, which suggests that IL-6 might function by depleting an intracellular thiol cofactor, perhaps GSH. Acetylcysteine 19-22 interleukin 6 Homo sapiens 205-209 23675187-4 2010 In addition, N-acetyl cysteine, a scavenger of reactive oxygen species, inhibits activation of NF-kappaB and induction of interleukin-6 by tumor necrosis factor alpha, being ineffective on interleukin-1 beta activity. Acetylcysteine 13-30 interleukin 6 Homo sapiens 122-135 21131394-10 2011 The changes in oxidant/antioxidant enzymes and IL-6 release were reversed by the antioxidants N-acetyl-cysteine (NAC) and ebselen through inhibition of Smad3 phosphorylation, indicating redox-dependent activation of Smad3 by TGF-beta. Acetylcysteine 94-111 interleukin 6 Homo sapiens 47-51 21131394-10 2011 The changes in oxidant/antioxidant enzymes and IL-6 release were reversed by the antioxidants N-acetyl-cysteine (NAC) and ebselen through inhibition of Smad3 phosphorylation, indicating redox-dependent activation of Smad3 by TGF-beta. Acetylcysteine 113-116 interleukin 6 Homo sapiens 47-51 14605526-14 2003 CONCLUSIONS: Administration of N-acetylcysteine results in decreased nuclear factor-kappa B activation in patients with sepsis, associated with decreases in interleukin-8 but not interleukin-6 or soluble intercellular adhesion molecule-1. Acetylcysteine 31-47 interleukin 6 Homo sapiens 179-192 18617679-5 2009 Pretreatment with N-acetylcysteine (NAC) or EUK-134, in a dose-dependent manner, attenuated PM-induced ROS production, COX-2 expression, and IL-6 release. Acetylcysteine 18-34 interleukin 6 Homo sapiens 141-145 18617679-5 2009 Pretreatment with N-acetylcysteine (NAC) or EUK-134, in a dose-dependent manner, attenuated PM-induced ROS production, COX-2 expression, and IL-6 release. Acetylcysteine 36-39 interleukin 6 Homo sapiens 141-145 14982601-6 2004 Stretch-induced IL-8 and IL-6 production were significantly inhibited when intracellular GSH was further increased by NAC or GSH-e (P < 0.0001). Acetylcysteine 118-121 interleukin 6 Homo sapiens 25-29 17521393-0 2007 Mycobacterium tuberculosis H37Rv induces monocytic release of interleukin-6 via activation of mitogen-activated protein kinases: inhibition by N-acetyl-L-cysteine. Acetylcysteine 143-162 interleukin 6 Homo sapiens 62-75 17521393-3 2007 The aim of this study was to investigate the role of mitogen-activated protein kinases in the secretion of interleukin-6 in THP-1 cells and human primary monocytes that were infected with Mycobacterium tuberculosis H37Rv, and its regulation by N-acetyl-L-cysteine, a potential antimycobacterial agent. Acetylcysteine 244-263 interleukin 6 Homo sapiens 107-120 17521393-6 2007 Pretreatment with N-acetyl-L-cysteine reduced, in a dose-dependent manner, M. tuberculosis H37Rv-induced activation of mitogen-activated protein kinase kinase 3/6 and interleukin-6 production in THP-1 cells. Acetylcysteine 18-37 interleukin 6 Homo sapiens 167-180 12679464-9 2003 Treatment of fetal membranes with NAC significantly suppressed lipopolysaccharide-stimulated type II phospholipase A(2) release and content; PGF(2alpha), IL-6, IL-8, TNFalpha, and 8-isoprostane release; and matrix metalloproteinase-9 and urokinase-type plasminogen activator enzyme activity and suppressed NF-kappaB DNA-binding activity (by ANOVA, P < 0.05). Acetylcysteine 34-37 interleukin 6 Homo sapiens 154-158 12832326-8 2003 N-acetylcysteine (NAC) prevented the IL-6 secretion in acetoacetate-treated U937 monocytes. Acetylcysteine 0-16 interleukin 6 Homo sapiens 37-41 12832326-8 2003 N-acetylcysteine (NAC) prevented the IL-6 secretion in acetoacetate-treated U937 monocytes. Acetylcysteine 18-21 interleukin 6 Homo sapiens 37-41 12832326-9 2003 CONCLUSIONS: This study demonstrates that hyperketonemia increases IL-6 levels in the blood of type 1 diabetic patients and that NAC can inhibit IL-6 secretion by U937 monocytic cells cultured in a ketotic medium. Acetylcysteine 129-132 interleukin 6 Homo sapiens 145-149 11799073-9 2002 Incubation of VSMCs with the antioxidant N-acetylcysteine suppressed GSA-elicited mRNA induction of MCP-1 and IL-6. Acetylcysteine 41-57 interleukin 6 Homo sapiens 110-114 11597988-4 2001 We first confirmed that antioxidant N-acetylcysteine, superoxide scavenger Tiron, and DPI suppressed Ang II-induced IL-6 expression. Acetylcysteine 36-52 interleukin 6 Homo sapiens 116-120 10925209-5 2000 The thiol antioxidant, N-acetylcysteine (NAC) abolished the synergism between IL-1beta or IL-6 and 1,25(OH)(2)D(3), but had only a small protective effect when the cytokines acted alone. Acetylcysteine 23-39 interleukin 6 Homo sapiens 90-100 11024008-6 2000 C5b-9 also induced formation of reactive oxygen species, which, along with IL-6 release, was inhibited by the antioxidant N-acetylcysteine. Acetylcysteine 122-138 interleukin 6 Homo sapiens 75-79 10708808-6 2000 Also, IL-6 stimulated the proliferation of FLSs, and this IL-6 driven proliferation was inhibited with the treatment of MTX or N-acetylcysteine (NAC, 1 mM). Acetylcysteine 127-143 interleukin 6 Homo sapiens 6-10 10708808-6 2000 Also, IL-6 stimulated the proliferation of FLSs, and this IL-6 driven proliferation was inhibited with the treatment of MTX or N-acetylcysteine (NAC, 1 mM). Acetylcysteine 127-143 interleukin 6 Homo sapiens 58-62 10708808-6 2000 Also, IL-6 stimulated the proliferation of FLSs, and this IL-6 driven proliferation was inhibited with the treatment of MTX or N-acetylcysteine (NAC, 1 mM). Acetylcysteine 145-148 interleukin 6 Homo sapiens 6-10 10708808-6 2000 Also, IL-6 stimulated the proliferation of FLSs, and this IL-6 driven proliferation was inhibited with the treatment of MTX or N-acetylcysteine (NAC, 1 mM). Acetylcysteine 145-148 interleukin 6 Homo sapiens 58-62 10708808-7 2000 Furthermore, ROS production in FLSs was increased significantly by IL-6, and its effect was also abrogated in the presence of MTX or NAC. Acetylcysteine 133-136 interleukin 6 Homo sapiens 67-71 10489835-6 1999 Addition of GSH and NAC significantly reduced the secretion of TNF-alpha (mean+/-SEM 21.2+/-5 and 44.7+/-4.4% inhibition, respectively) as well as LPS-induced IL-6 and IL-8 (p<0.05). Acetylcysteine 20-23 interleukin 6 Homo sapiens 159-163 10403520-8 1999 The treatment of A2780 cells with N-acetyl-L-cysteine increased the intracellular GSH concentration, and profoundly suppressed hsp72 mRNA induction and HSF activation by CdCl2. Acetylcysteine 34-53 interleukin 6 Homo sapiens 152-155 10489835-7 1999 Similarly, NAC inhibited the production of TNF-alpha, IL-6 and IL-8 in GSH-depleted AMs obtained by BSO pretreatment. Acetylcysteine 11-14 interleukin 6 Homo sapiens 54-58 10489835-8 1999 In conclusion, N-acetylcysteine and glutathione inhibit the production of tumour necrosis factor-alpha, interleukin-8 and interleukin-6 by alveolar macrophages by a mechanism independent of glutathione metabolism. Acetylcysteine 15-31 interleukin 6 Homo sapiens 122-135 9651185-8 1998 The IL-6 response was inhibited by the metal chelator deferoxamine and the free radical scavenger N-acetyl-L-cysteine, suggesting that the activation of NF-kappaB may be mediated through reactive oxygen intermediates generated by transition metals found in ROFA. Acetylcysteine 98-117 interleukin 6 Homo sapiens 4-8 9378980-3 1997 IL-6 induction was dependent on the intracellular redox-oxidative state, since intracellular hydroxyl scavengers and N-acetylcysteine, a precursor of glutathione, abrogated IL-6 secretion by asbestos or H2O2. Acetylcysteine 117-133 interleukin 6 Homo sapiens 0-4 9378980-3 1997 IL-6 induction was dependent on the intracellular redox-oxidative state, since intracellular hydroxyl scavengers and N-acetylcysteine, a precursor of glutathione, abrogated IL-6 secretion by asbestos or H2O2. Acetylcysteine 117-133 interleukin 6 Homo sapiens 173-177 8896414-4 1996 Both PDTC and NAC inhibited, in a dose-dependent manner, the synthesis of IL-6, IL-8, and GM-CSF induced by tumor necrosis factor (TNF)-alpha or bacterial lipopolysaccharides (LPS) in human umbilical vein endothelial cells (HUVEC). Acetylcysteine 14-17 interleukin 6 Homo sapiens 74-78