PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 19116908-8 2009 Moreover, oral nicotine inhibited bone degradation and reduced TNFalpha expression in synovial tissue. Nicotine 15-23 tumor necrosis factor Mus musculus 63-71 19626424-6 2010 Furthermore, we examined the ability of the cells to release cytokine when stimulated with both nicotine and LPS and showed that the stimulation with LPS augmented the secretion of IL-1a, IL-1b, IL-6, and TNF-alpha. Nicotine 96-104 tumor necrosis factor Mus musculus 205-214 19209239-8 2009 Nicotine administration 2 h after ricin injection significantly delayed and reduced ricin-induced mortality, an effect coupled with reduced serum levels of tumor necrosis factor-alpha and markers of kidney and liver dysfunction. Nicotine 0-8 tumor necrosis factor Mus musculus 156-183 16254210-5 2006 We quantified 18 different serum cytokines and found a significant increase of tumor necrosis factor alpha, interleukin 1beta, and keratinocyte-derived chemokine in nicotine-treated mice. Nicotine 165-173 tumor necrosis factor Mus musculus 79-106 17520028-7 2007 Additionally, nicotine significantly reduced tubular damages, prevented neutrophil infiltration and decreased productions of the CXC-chemokine KC, TNF-alpha and the proinflammatory high-mobility group box 1 protein. Nicotine 14-22 tumor necrosis factor Mus musculus 147-156 16254210-7 2006 At the cellular level, nicotine induced tumor necrosis factor alpha and inducible nitric oxide synthase expression in RAW264.7 cells via the nicotinic acetylcholine receptors. Nicotine 23-31 tumor necrosis factor Mus musculus 40-67 10549987-6 1999 We have shown previously that nicotine, acting through an alpha-bungarotoxin sensitive receptor, is also neuroprotective, but it too specifically abolishes TNFalpha-mediated neuroprotection. Nicotine 30-38 tumor necrosis factor Mus musculus 156-164 15056277-7 2004 Acetylcholine and nicotine pre-treatment inhibit lipopolysaccharide (LPS)-induced TNF-alpha release in murine-derived microglial cells, an effect attenuated by alpha 7 selective nicotinic antagonist, alpha-bungarotoxin. Nicotine 18-26 tumor necrosis factor Mus musculus 82-91 14622092-3 2003 The inflammatory cytokine tumor necrosis factor alpha (TNFalpha) is also neuroprotective, however, in the presence of nicotine, neuroprotection against NMDA is abolished. Nicotine 118-126 tumor necrosis factor Mus musculus 26-53 14622092-3 2003 The inflammatory cytokine tumor necrosis factor alpha (TNFalpha) is also neuroprotective, however, in the presence of nicotine, neuroprotection against NMDA is abolished. Nicotine 118-126 tumor necrosis factor Mus musculus 55-63 14622092-4 2003 The specificity of nicotine-TNFalpha antagonism was further refined using a mouse transgenic dominant negative of nAChRalpha7 in which nicotine failed to induce neuroprotection against NMDA and antagonism of TNFalpha was absent. Nicotine 19-27 tumor necrosis factor Mus musculus 28-36 14622092-6 2003 The mechanism of TNFalpha-mediated neuroprotection and antagonism by nicotine was independent of caspase 8 activation or nuclear factor kappa B translocation in neurons but C6-ceramide addition to neuronal cultures subsequently exposed to NMDA mimicked the neuroprotective effect of TNFalpha and, like TNFalpha, it was antagonized by cotreatment with nicotine. Nicotine 69-77 tumor necrosis factor Mus musculus 17-25 14622092-6 2003 The mechanism of TNFalpha-mediated neuroprotection and antagonism by nicotine was independent of caspase 8 activation or nuclear factor kappa B translocation in neurons but C6-ceramide addition to neuronal cultures subsequently exposed to NMDA mimicked the neuroprotective effect of TNFalpha and, like TNFalpha, it was antagonized by cotreatment with nicotine. Nicotine 69-77 tumor necrosis factor Mus musculus 283-291 14622092-6 2003 The mechanism of TNFalpha-mediated neuroprotection and antagonism by nicotine was independent of caspase 8 activation or nuclear factor kappa B translocation in neurons but C6-ceramide addition to neuronal cultures subsequently exposed to NMDA mimicked the neuroprotective effect of TNFalpha and, like TNFalpha, it was antagonized by cotreatment with nicotine. Nicotine 69-77 tumor necrosis factor Mus musculus 283-291 14622092-6 2003 The mechanism of TNFalpha-mediated neuroprotection and antagonism by nicotine was independent of caspase 8 activation or nuclear factor kappa B translocation in neurons but C6-ceramide addition to neuronal cultures subsequently exposed to NMDA mimicked the neuroprotective effect of TNFalpha and, like TNFalpha, it was antagonized by cotreatment with nicotine. Nicotine 351-359 tumor necrosis factor Mus musculus 17-25 10727751-7 2000 TNF-alpha and IL-6 production were significantly enhanced by 1 microg/ml of nicotine when cells were pre-incubated with nicotine for 3 h compared to concurrent incubation relative to LPS stimulation. Nicotine 76-84 tumor necrosis factor Mus musculus 0-9 10727751-7 2000 TNF-alpha and IL-6 production were significantly enhanced by 1 microg/ml of nicotine when cells were pre-incubated with nicotine for 3 h compared to concurrent incubation relative to LPS stimulation. Nicotine 120-128 tumor necrosis factor Mus musculus 0-9 10727751-9 2000 TNF-alpha production was significantly inhibited by nicotine in young mice, while IL-6 production was significantly inhibited by nicotine in old mice. Nicotine 52-60 tumor necrosis factor Mus musculus 0-9 29901817-10 2018 In vitro study, the TNF-alpha-enhanced mRNA expression of MAdCAM-1 was reduced by the coadministration of nicotine in a dose-dependent manner, possibly via nicotinic receptor activation. Nicotine 106-114 tumor necrosis factor Mus musculus 20-29 34557761-8 2021 In keeping with targeting MD2, both nicotine and cotinine inhibited LPS-induced production of nitric oxide and tumor necrosis factor alpha (TNF-alpha) and blocked microglial activation. Nicotine 36-44 tumor necrosis factor Mus musculus 111-138 34557761-8 2021 In keeping with targeting MD2, both nicotine and cotinine inhibited LPS-induced production of nitric oxide and tumor necrosis factor alpha (TNF-alpha) and blocked microglial activation. Nicotine 36-44 tumor necrosis factor Mus musculus 140-149 30391635-8 2019 Notably, flow cytometric analysis also revealed an enhancement of TNFalpha and IFNgamma plasmatic levels at the same time point during nicotine withdrawal. Nicotine 135-143 tumor necrosis factor Mus musculus 66-74 34220004-4 2021 Nicotine-treated and control mice were sacrificed 6, 16 and 24 weeks post-treatment, and their tissues evaluated for alterations in histology, oxidative stress, TNF-alpha levels, nitric oxide (NO) and myeloperoxidase (MPO) release, tumor suppressor response and DNA repair response. Nicotine 0-8 tumor necrosis factor Mus musculus 161-170 34220004-6 2021 The tissues of nicotine treated mice exhibited a large number of multinucleated and binucleated cells, enlarged nuclei and non-uniform distribution of cells, significant increase in expression of TNF-alpha gene and serum TNF-alpha, and time-dependent significant increase in lipid peroxidation, protein carbonylation, NO and MPO release when compared to age-and gender-matched controls. Nicotine 15-23 tumor necrosis factor Mus musculus 196-205 34220004-6 2021 The tissues of nicotine treated mice exhibited a large number of multinucleated and binucleated cells, enlarged nuclei and non-uniform distribution of cells, significant increase in expression of TNF-alpha gene and serum TNF-alpha, and time-dependent significant increase in lipid peroxidation, protein carbonylation, NO and MPO release when compared to age-and gender-matched controls. Nicotine 15-23 tumor necrosis factor Mus musculus 221-230 30085294-7 2019 However, plasma TNFalpha levels were significantly increased in mice exposed to Copenhagen snuff or nicotine for 24 weeks. Nicotine 100-108 tumor necrosis factor Mus musculus 16-24 30085294-14 2019 Increased formation of proinflammatory cytokines such as TNFalpha by nicotine or Copenhagen snuff may lead to vascular inflammation and thereby exacerbate atherogenesis. Nicotine 69-77 tumor necrosis factor Mus musculus 57-65 29470537-8 2018 In addition, nicotine inhibited TNFalpha release by LPS activated mPGES-1 (+/+) splenocytes in vitro. Nicotine 13-21 tumor necrosis factor Mus musculus 32-40 29906478-6 2018 Increased oxidative stress by tramadol and/or nicotine sequentially augmented nuclear factor kappa B and the proinflammatory cytokine tumor necrosis factor alpha with the induction of apoptosis evident by the increased caspase-3 immunoreactivity. Nicotine 46-54 tumor necrosis factor Mus musculus 134-161 28960086-8 2018 In the mothers" lungs, e-cigarette exposure with and without nicotine increased the proinflammatory cytokines IL-1beta, IL-6, and TNF-alpha. Nicotine 61-69 tumor necrosis factor Mus musculus 130-139 27752155-9 2016 The results of our investigation demonstrated that nicotine could reduce significantly the levels of IL-6, and TNF-alpha in serum (P<0.05). Nicotine 51-59 tumor necrosis factor Mus musculus 111-120 28013195-7 2017 Nicotine induced dose-dependent NETosis in ex vivo neutrophils from healthy non-smokers, and co-incubation with ACPA-immune complexes or TNF-alpha facilitated a synergistic effect on NETosis. Nicotine 0-8 tumor necrosis factor Mus musculus 137-146 27938563-5 2016 Results: The results of ELISA showed that compared with the endotoxin+nicotine group of C57 NASH mice, the endotoxin+nicotine group of gene knockout NASH mice had significantly higher levels of IL-6 and TNF-alpha in supernatant (IL-6: 1 599+-65 pg/ml vs 1 465+-45 pg/ml, P < 0.05; TNF-alpha: 1 567+-66 pg/ml vs 1 433+-50 pg/ml, P < 0.05). Nicotine 117-125 tumor necrosis factor Mus musculus 203-212 27938563-5 2016 Results: The results of ELISA showed that compared with the endotoxin+nicotine group of C57 NASH mice, the endotoxin+nicotine group of gene knockout NASH mice had significantly higher levels of IL-6 and TNF-alpha in supernatant (IL-6: 1 599+-65 pg/ml vs 1 465+-45 pg/ml, P < 0.05; TNF-alpha: 1 567+-66 pg/ml vs 1 433+-50 pg/ml, P < 0.05). Nicotine 117-125 tumor necrosis factor Mus musculus 284-293 25616906-7 2015 Nicotine downregulated production of IL-6 and MCP-1 in RA-FLSs induced by TNFalpha in a concentration-dependent manner, and IL-10 levels were not significantly different after nicotine pretreatment. Nicotine 0-8 tumor necrosis factor Mus musculus 74-82 26851533-8 2016 The proinflammatory cytokines TNF-alpha, IL-1beta, IL-6 and IL-17A were significantly decreased in the infected mice treated with nicotine compared with methyllycaconitine. Nicotine 130-138 tumor necrosis factor Mus musculus 30-39 26925951-8 2016 We thus confirmed this hypothesis by measuring cytokine expression, where we found that nicotine inhibited the production of the pro-inflammatory cytokines TNFalpha, IL-1beta and IL-12, while stimulating the secretion of IL-10, an anti-inflammatory cytokine. Nicotine 88-96 tumor necrosis factor Mus musculus 156-164 26607717-6 2016 TRIM27, an E3 ubiquitin ligase that activated TNF apoptotic pathway through up-regulating deubiquitinated RIP1, was also overexpressed in nicotine-treated spermatocytes; moreover, four consecutive CpG sites near the Trim27 transcription start site were less frequently methylated. Nicotine 138-146 tumor necrosis factor Mus musculus 46-49 26607717-8 2016 In summary, our study suggests that nicotine may induce murine spermatozoal apoptosis via the TNF apoptotic pathway through up-regulation of deubiquitinated RIP1 by Trim27 promoter hypomethylation. Nicotine 36-44 tumor necrosis factor Mus musculus 94-97 26397391-5 2015 Investigation of the underlying mechanism showed that nicotine reduced the secretion of the pro-inflammatory cytokines tumor necrosis factor alpha and interleukin 6 in vitro and in vivo. Nicotine 54-62 tumor necrosis factor Mus musculus 119-146 26507386-8 2015 The mRNA expressions and protein levels of TNF-alpha, IL-1beta, IL-6, and IL-17A were significantly downregulated in dose-dependent manners in the nicotine treatment groups compared to the infected untreated group. Nicotine 147-155 tumor necrosis factor Mus musculus 43-52 26607717-3 2016 Out of the 86 genes related to apoptosis, Tnf (tumor necrosis factor alpha) was screened to be the most significant varied transcript, and the Onto-pathway analysis indicated that the TNF apoptotic pathway was especially activated by nicotine exposure. Nicotine 234-242 tumor necrosis factor Mus musculus 42-45 26607717-3 2016 Out of the 86 genes related to apoptosis, Tnf (tumor necrosis factor alpha) was screened to be the most significant varied transcript, and the Onto-pathway analysis indicated that the TNF apoptotic pathway was especially activated by nicotine exposure. Nicotine 234-242 tumor necrosis factor Mus musculus 47-74 26607717-3 2016 Out of the 86 genes related to apoptosis, Tnf (tumor necrosis factor alpha) was screened to be the most significant varied transcript, and the Onto-pathway analysis indicated that the TNF apoptotic pathway was especially activated by nicotine exposure. Nicotine 234-242 tumor necrosis factor Mus musculus 184-187 26607717-5 2016 The results showed that RIP1, the key component in the TNF apoptotic pathway, was up-expressed in its deubiquitinated form in nicotine-treated mice testis. Nicotine 126-134 tumor necrosis factor Mus musculus 55-58 25396421-7 2014 Nicotine treatments significantly improved survival rate, attenuated myocardial lesions, and downregulated the expression of TNF-alpha and IL-6. Nicotine 0-8 tumor necrosis factor Mus musculus 125-134 25258409-10 2014 Nicotine markedly inhibited the elevation of TNF-alpha and IL-6 mRNA as well as phosphorylated signal transducer and activator of transcription (Stat) 3 expression in the colons of the tumor model mice. Nicotine 0-8 tumor necrosis factor Mus musculus 45-54 25258409-12 2014 Furthermore, it is presumed that nicotine downregulates the expression of inflammatory mediators such as IL-6/Stat3 and TNF-alpha, thereby reducing the colonic tumorigenesis associated with chronic colitis. Nicotine 33-41 tumor necrosis factor Mus musculus 120-129 25751390-7 2015 The degree of liver inflammation in the NASH mice decreased after nicotine administration, and the level of serum TNFa also significantly decreased. Nicotine 66-74 tumor necrosis factor Mus musculus 114-118 25751390-8 2015 The levels of serum TNFa were 21.95+/-0.8 pg/mL in nicotine-treated mice and 38.07+/-1.7 pg/mL in the non-nicotine-treated NASH mice (P less than 0.05). Nicotine 51-59 tumor necrosis factor Mus musculus 20-24 25751390-8 2015 The levels of serum TNFa were 21.95+/-0.8 pg/mL in nicotine-treated mice and 38.07+/-1.7 pg/mL in the non-nicotine-treated NASH mice (P less than 0.05). Nicotine 106-114 tumor necrosis factor Mus musculus 20-24 25751390-9 2015 The nicotine treatment also significantly reduced the concentration of TNFa in the culture supernatants of Kupffer cells after LPS stimulation; moreover, the supernatant level of TNFa decreased significantly after the nicotine treatment (Pless than 0.05). Nicotine 4-12 tumor necrosis factor Mus musculus 71-75 25751390-9 2015 The nicotine treatment also significantly reduced the concentration of TNFa in the culture supernatants of Kupffer cells after LPS stimulation; moreover, the supernatant level of TNFa decreased significantly after the nicotine treatment (Pless than 0.05). Nicotine 218-226 tumor necrosis factor Mus musculus 179-183 24313917-8 2014 Moreover, serum TNFalpha levels were lower in the nicotine-treated group. Nicotine 50-58 tumor necrosis factor Mus musculus 16-24 24669857-5 2014 Nicotine"s effect on the expression of cell surface Toll-like receptors (TLRs), MCP-1, COX-2, and TNF-alpha were examined by real-time PCR. Nicotine 0-8 tumor necrosis factor Mus musculus 98-107 21239632-4 2011 An analysis of the phenotype of isolated brain microvessels after nicotine exposure indicated higher expression of inflammatory mediators, cytokines (IL-1beta, TNF-alpha, and IL-18), chemokines (CCL2 and CX(3)CL1), and adhesion molecules (ICAM-1, VCAM-1, and P-selectins), and this was accompanied by enhanced leukocyte infiltration into brain during ischemia/reperfusion (P < 0.01). Nicotine 66-74 tumor necrosis factor Mus musculus 160-169 23028093-2 2013 Of 51 genes expressed in the Toll-like receptor (TLR) and RIG-I-like receptor (RLR) pathways, mRNA expression of 15 genes in RAW264.7 cells was attenuated by nicotine, of which mRNA expression of IL-6, TNF-alpha, and IL-1beta was confirmed to be attenuated in peritoneal macrophages. Nicotine 158-166 tumor necrosis factor Mus musculus 202-211 23028093-3 2013 Concurrently, nicotine treatment attenuated the release of IL-6 and TNF-alpha from poly(I:C)-stimulated macrophages. Nicotine 14-22 tumor necrosis factor Mus musculus 68-77 23028093-4 2013 However, when poly(I:C)-stimulated macrophages were challenged with nicotine plus alpha-bungarotoxin (alpha-BTX), secretion of IL-6 and TNF-alpha was found to be in a level seen with poly(I:C) stimulation only, indicating that alpha7-nAChR, a highly Ca(2+) permeable ion channel sensitive to blockade by alpha-BTX, is involved in this process. Nicotine 68-76 tumor necrosis factor Mus musculus 136-145 22926197-0 2012 Tnfalpha, Cox2 and AdipoQ adipokine gene expression levels are modulated in murine adipose tissues by both nicotine and nACh receptors containing the beta2 subunit. Nicotine 107-115 tumor necrosis factor Mus musculus 0-8 22926197-4 2012 Additionally, when nicotine was administered to wild-type mice, it significantly affected the expression of adipokine genes, such as Tnfalpha, AdipoQ, Haptoglobin and Mcp1 in WAT. Nicotine 19-27 tumor necrosis factor Mus musculus 133-141 22926197-6 2012 Furthermore, interactions between mouse beta2 subunit and nicotine treatment affected the expression levels of the adipokine genes Tnfalpha, Cox2 and AdipoQ in WAT and of AdipoQ in BAT. Nicotine 58-66 tumor necrosis factor Mus musculus 131-139 22624500-8 2012 In primary cultured mouse astrocytes, pretreatment with nicotine suppressed MPP(+)-induced or LPS-induced astrocyte activation, as evidenced by both decreased production of TNF-alpha and inhibition of extracellular regulated kinase1/2 (Erk1/2) and p38 activation in astrocytes, and these effects were also reversed by MLA. Nicotine 56-64 tumor necrosis factor Mus musculus 173-182 22803143-1 2012 Experiments on outbred albino mice have shown that proserine (reversible cholinesterase inhibitor) and nicotine (nicotinic receptor agonist) in a equivalent dose of 0.2 DL(50)injected 2 h before sepsis induction significantly reduced animal mortality from experimental infection due to reduction of blood concentrations of proinflammatory cytokines TNF-alpha, IL-1beta, and IL-6. Nicotine 103-111 tumor necrosis factor Mus musculus 349-358 23737837-3 2013 Embryos exposed to nicotine (1 mM) exhibited severe morphological anomalies and apoptotic cell death, as well as increased levels of TNF- alpha , IL-1 beta , and caspase 3 mRNAs, and lipid peroxidation. Nicotine 19-27 tumor necrosis factor Mus musculus 133-143 20664191-8 2011 RESULTS: Nicotine pretreatment significantly attenuated the severity of lung injury and inhibited the production of TNF-alpha, IL-1beta and HMGB-1 in mice with ALI. Nicotine 9-17 tumor necrosis factor Mus musculus 116-125 21239433-7 2011 Nicotine significantly suppressed free fatty acid- and TNFalpha-induced cytokine production in wild type (WT), but not alpha7KO macrophages. Nicotine 0-8 tumor necrosis factor Mus musculus 55-63 20615555-4 2010 In vivo treatment with nicotine attenuated muscular inflammation characterized by reduced metalloprotease MMP-9 activity, TNFalpha and NFkB content and increased muscular regeneration. Nicotine 23-31 tumor necrosis factor Mus musculus 122-130 19890701-11 2010 Expression of TNF-alpha and IL-6 decreased in nicotine-pretreated mice compared with model and vagotomy mice; IL-10 levels were not significantly different between the model group and nicotine group. Nicotine 46-54 tumor necrosis factor Mus musculus 14-23