PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 11544433-0 2001 N-acetylcysteine attenuates the increase in alpha-glutathione S-transferase and circulating ICAM-1 and VCAM-1 after reperfusion in humans undergoing liver transplantation. Acetylcysteine 0-16 vascular cell adhesion molecule 1 Homo sapiens 103-109 11557664-7 2001 13-HPODE-induced nuclear factor-kappaB DNA binding activity was blocked by an antioxidant, N-acetylcysteine, as well as an inhibitor of protein kinase C. 13-HPODE, but not the hydroxy product, 13-(S)-hydroxyoctadecadienoic acid, also dose-dependently increased vascular cell adhesion molecule-1 promoter activation. Acetylcysteine 91-107 vascular cell adhesion molecule 1 Homo sapiens 261-294 11544433-10 2001 CONCLUSIONS: NAC attenuated the increase in alpha-glutathione S-transferase and circulating ICAM-1 and VCAM-1 after reperfusion of the donor liver, indicating possible cytoprotective effects of NAC. Acetylcysteine 13-16 vascular cell adhesion molecule 1 Homo sapiens 103-109 11133225-8 2001 Pretreatment of HUVEC with pyrrolidine dithiocarbamate (PDTC) or N-acetylcysteine (NAC) completely prevented IL-4-induced VCAM-1 expression. Acetylcysteine 65-81 vascular cell adhesion molecule 1 Homo sapiens 122-128 11133225-8 2001 Pretreatment of HUVEC with pyrrolidine dithiocarbamate (PDTC) or N-acetylcysteine (NAC) completely prevented IL-4-induced VCAM-1 expression. Acetylcysteine 83-86 vascular cell adhesion molecule 1 Homo sapiens 122-128 10362686-9 1999 Moreover, the oxygen-induced rise could be mimicked by addition of H2O2 to normoxic cells, and the oxygen-induced expression of VCAM-1 but not of ICAM-1 was inhibited by addition of the free radical scavengers superoxide dismutase, N-acetyl-L-cysteine, and pyrrolidinedithiocarbamate. Acetylcysteine 232-251 vascular cell adhesion molecule 1 Homo sapiens 128-134 9833950-0 1998 Reduction of oxidative stress by oral N-acetyl-L-cysteine treatment decreases plasma soluble vascular cell adhesion molecule-1 concentrations in non-obese, non-dyslipidaemic, normotensive, patients with non-insulin-dependent diabetes. Acetylcysteine 38-57 vascular cell adhesion molecule 1 Homo sapiens 93-126 9833950-7 1998 Treatment with N-acetyl-L-cysteine decreased plasma VCAM-1 (p = 0.01) and intraerythrocytic GSSG (p = 0.006) but increased GSH concentrations (p = 0.04) and the GSH:GSSG ratio (p = 0.004) in non-insulin dependent diabetic patients. Acetylcysteine 15-34 vascular cell adhesion molecule 1 Homo sapiens 52-58 7522548-4 1994 PDTC or N-acetylcysteine dose dependently reduced TNF-induced VCAM-1 but not ICAM-1 surface protein (also in human umbilical arterial endothelial cells) and mRNA expression (by 70% at 100 mumol/L PDTC) in HUVECs as assessed by flow cytometry and polymerase chain reaction. Acetylcysteine 8-24 vascular cell adhesion molecule 1 Homo sapiens 62-68 9529157-11 1998 Experiments performed in the presence of the antioxidant N-acetylcysteine demonstrated that the expression of vascular cell adhesion molecule-1 could be almost totally abolished, whereas that of intercellular adhesion molecule-1 was typically reduced by approximately 70%. Acetylcysteine 57-73 vascular cell adhesion molecule 1 Homo sapiens 110-143 9277499-0 1997 Distinct mechanisms for N-acetylcysteine inhibition of cytokine-induced E-selectin and VCAM-1 expression. Acetylcysteine 24-40 vascular cell adhesion molecule 1 Homo sapiens 87-93 7544803-5 1995 The inhibitory effect of anti-RAGE IgG, a truncated form of the receptor (soluble RAGE) or N-acetylcysteine on VCAM-1 expression indicated that AGE-RAGE-induced oxidant stress was central to VCAM-1 induction. Acetylcysteine 91-107 vascular cell adhesion molecule 1 Homo sapiens 111-117 7544803-5 1995 The inhibitory effect of anti-RAGE IgG, a truncated form of the receptor (soluble RAGE) or N-acetylcysteine on VCAM-1 expression indicated that AGE-RAGE-induced oxidant stress was central to VCAM-1 induction. Acetylcysteine 91-107 vascular cell adhesion molecule 1 Homo sapiens 191-197 7544803-6 1995 Electrophoretic mobility shift assays on nuclear extracts from AGE-treated ECs showed induction of specific DNA binding activity for NF-kB in the VCAM-1 promoter, which was blocked by anti-RAGE IgG or N-acetylcysteine. Acetylcysteine 201-217 vascular cell adhesion molecule 1 Homo sapiens 146-152 7691889-3 1993 In cultured human umbilical vein endothelial (HUVE) cells, the cytokine interleukin 1 beta (IL-1 beta) activated VCAM-1 gene expression through a mechanism that was repressed approximately 90% by the antioxidants pyrrolidine dithiocarbamate (PDTC) and N-acetylcysteine (NAC). Acetylcysteine 252-268 vascular cell adhesion molecule 1 Homo sapiens 113-119 7521369-12 1994 The induction of VCAM-1 but not of ICAM-1 proved susceptible to inhibition by both PDTC and NAC. Acetylcysteine 92-95 vascular cell adhesion molecule 1 Homo sapiens 17-23 7691889-3 1993 In cultured human umbilical vein endothelial (HUVE) cells, the cytokine interleukin 1 beta (IL-1 beta) activated VCAM-1 gene expression through a mechanism that was repressed approximately 90% by the antioxidants pyrrolidine dithiocarbamate (PDTC) and N-acetylcysteine (NAC). Acetylcysteine 270-273 vascular cell adhesion molecule 1 Homo sapiens 113-119 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 vascular cell adhesion molecule 1 Homo sapiens 235-241 27206739-7 2016 Sal, PBA, NAC and inhibitors of p38 MAP kinase and NF-kB induced the decrease of VCAM-1 expression and of the ensuing monocyte adhesion induced by gLDL. Acetylcysteine 10-13 vascular cell adhesion molecule 1 Homo sapiens 81-87 29328400-6 2018 Nacetylcysteine, a Nox4 inhibitor, was demonstrated to inhibit ROS generation, suppress VCAM-1 and ICAM-1 protein expression, and decrease oxidative stress and inflammation in HK-2 cells following overexpression of miR-146a. Acetylcysteine 0-15 vascular cell adhesion molecule 1 Homo sapiens 88-94 26707483-7 2016 Endothelial VCAM-1 induction by TNF-alpha was responsible for superoxide anion production being quenched by N-acetyl-cysteine and Tat-SOD. Acetylcysteine 108-125 vascular cell adhesion molecule 1 Homo sapiens 12-18 25876056-6 2016 However, N-acetylcysteine (NAC), a scavenger of ROS, prevented the increase of ROS generation, attenuated the phosphorylation of the above kinases, and decreased the NF-kappaB activation as well as the expression of ICAM-1 and VCAM-1. Acetylcysteine 9-25 vascular cell adhesion molecule 1 Homo sapiens 227-233 25876056-6 2016 However, N-acetylcysteine (NAC), a scavenger of ROS, prevented the increase of ROS generation, attenuated the phosphorylation of the above kinases, and decreased the NF-kappaB activation as well as the expression of ICAM-1 and VCAM-1. Acetylcysteine 27-30 vascular cell adhesion molecule 1 Homo sapiens 227-233 22581648-9 2012 In addition, an antioxidant N-acetylcysteine mimicked the effects of GIP on RAGE and VCAM-1 gene expression in HUVECs. Acetylcysteine 28-44 vascular cell adhesion molecule 1 Homo sapiens 85-91 21767632-3 2011 The TNF-alpha-induced expression of VCAM-1 was significantly reduced by respectively 38+-7 or 34+-16% when HUVECs were pretreated with 10 or 30muM viscolin, as shown by Western blotting, and was also significantly reduced by pretreatment with the antioxidants N-acetylcysteine, diphenylene iodonium chloride, and apocynin. Acetylcysteine 260-276 vascular cell adhesion molecule 1 Homo sapiens 36-42 21236267-5 2011 Irbesartan or an anti-oxidant N-acetylcysteine inhibited the AGE-induced increase in reactive oxygen species (ROS) generation and subsequently blocked up-regulation of VCAM-1 mRNA levels in glomerular ECs. Acetylcysteine 30-46 vascular cell adhesion molecule 1 Homo sapiens 168-174 17334226-8 2007 Inhibition of Tat-induced ROS generation by N-acetyl cysteine, vitamin C and diphenyl iodonium suppressed Tat-induced NF-kappaB activation, ICAM-1 and VCAM-1 expression, and monocyte adhesion in CRT-MG. Acetylcysteine 44-61 vascular cell adhesion molecule 1 Homo sapiens 151-157 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 vascular cell adhesion molecule 1 Homo sapiens 174-180