PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 28986583-6 2017 Nicotine at 10 micromol/L significantly downregulated the release of TNF-alpha, but showed a lesser effect on IL-8 secretion and no effect on TGF-beta. Nicotine 0-8 tumor necrosis factor Homo sapiens 69-78 32370298-10 2020 Further treatment of these macrophages with nicotine or HLE extracts caused higher inflammatory response (increased iNOS (M1), TNF-alpha, IL-6, and M1/M2 ratio, p < 0.05), increased MAP burden, and decreased apoptosis. Nicotine 44-52 tumor necrosis factor Homo sapiens 127-136 31631328-6 2020 Moreover, it was observed that nicotine decreases the production of interleukin (IL)-6 and C-C chemokine ligand (CCL)5 during Mtb infection in epithelial cells (EpCs), whereas in macrophages derived from human monocytes (MDMs) there is a decrease in IL-8, IL-6, tumor necrosis factor (TNF)-alpha, IL-10, CCL2, C-X-C chemokine ligand (CXCL)9 and CXCL10 only during infection with Mtb. Nicotine 31-39 tumor necrosis factor Homo sapiens 262-295 30319609-3 2018 Results: The results of this study showed that monocyte induced inflammation (raised tumor necrosis factor-alpha-TNF-alpha) induced by mCRP was significantly blocked in the presence of acetylcholine and nicotine, whilst tacrine and targeted antibodies (clones 8C10 and 3H12) had less of or no significant effects. Nicotine 203-211 tumor necrosis factor Homo sapiens 85-112 30319609-3 2018 Results: The results of this study showed that monocyte induced inflammation (raised tumor necrosis factor-alpha-TNF-alpha) induced by mCRP was significantly blocked in the presence of acetylcholine and nicotine, whilst tacrine and targeted antibodies (clones 8C10 and 3H12) had less of or no significant effects. Nicotine 203-211 tumor necrosis factor Homo sapiens 113-122 30537800-6 2018 We have found that nicotine (at concentration 0.01microM) induced release of TNF-a and IL-6 but not CXCL-8 production. Nicotine 19-27 tumor necrosis factor Homo sapiens 77-82 28407244-6 2018 A slight downregulation of NFkB pathway and an increase in the production of TNF-alpha and, particularly PGE2, were involved in the observed effects of nicotine. Nicotine 152-160 tumor necrosis factor Homo sapiens 77-86 29658573-7 2018 The results indicated that A549 had increased levels of IL-6, IL-8 and TNF-alpha when cultured with nicotine when compared with the control cells. Nicotine 100-108 tumor necrosis factor Homo sapiens 71-80 26884647-5 2016 RESULTS: We found that nicotine reduced the levels of M1 state markers, including inducible nitric oxide synthase (iNOS) expression and tumor necrosis factor alpha (TNF-alpha) and interleukin- (IL-) 6 releases; meanwhile, it increased the levels of M2 state markers, including arginase-1 (Arg-1) expression and brain-derived neurotrophic factor (BDNF) release, in the Abeta-stimulated microglia. Nicotine 23-31 tumor necrosis factor Homo sapiens 136-163 27984197-5 2017 The results indicated that chronic nicotine administration (0.1mg/kg, s.c., 14days) inhibited the LPS-induced nuclear binding of NF-kappaB and mRNA expression levels of Tnf, Il1b, Nos2, and Tlr4. Nicotine 35-43 tumor necrosis factor Homo sapiens 169-172 27681882-11 2016 RESULTS: Nicotine treatment dose dependently limits the production of critical proinflammatory cytokines such as IL-6 (60.5 +- 3.3, %inhibition), IL-1beta (42.4 +- 1.7, %inhibition), and TNF-alpha (68.9 +- 7.7, %inhibition) by activated human astrocytes. Nicotine 9-17 tumor necrosis factor Homo sapiens 187-196 26884647-5 2016 RESULTS: We found that nicotine reduced the levels of M1 state markers, including inducible nitric oxide synthase (iNOS) expression and tumor necrosis factor alpha (TNF-alpha) and interleukin- (IL-) 6 releases; meanwhile, it increased the levels of M2 state markers, including arginase-1 (Arg-1) expression and brain-derived neurotrophic factor (BDNF) release, in the Abeta-stimulated microglia. Nicotine 23-31 tumor necrosis factor Homo sapiens 165-174 24287167-9 2014 Nicotine alone impaired IL-10 and TNF-alpha production by 48.8 (37)% and 49 (50)%, respectively (p<0.05) through an alpha-7 nicotine receptor-independent mechanism. Nicotine 0-8 tumor necrosis factor Homo sapiens 34-43 26334245-9 2015 Pharmacologic and siRNA-mediated inhibition of PLD1 and PLD2 attenuated the nicotine- and LPS-induced upregulation of inducible nitric oxide (NO) synthase and cyclooxygenase-2, production of NO, and prostaglandin E2, and mRNA expression and secretion of tumor necrosis factor-alpha, interleukin (IL)-1beta, and IL-8. Nicotine 76-84 tumor necrosis factor Homo sapiens 254-281 25259522-6 2014 Moreover, down-regulation of this expression by small interfering RNAs specific to the IRAK-M gene significantly reverses the anti-inflammatory effect of nicotine on LPS-induced TNF-alpha production. Nicotine 154-162 tumor necrosis factor Homo sapiens 178-187 25259522-7 2014 Interestingly, macrophages pre-exposed to nicotine exhibit higher IRAK-M levels and reduced TNF-alpha response to an additional LPS challenge, a behavior reminiscent of the "endotoxin tolerant" phenotype identified in monocytes either pre-exposed to LPS or from immunocompromised septic patients. Nicotine 42-50 tumor necrosis factor Homo sapiens 92-101 22095388-9 2012 Cells pretreated with nicotine prior to lipopolysaccharide (LPS) stimulation exhibited a lower production of TNF-alpha, IL-8, and IL-6 compared to LPS-treated (only) cells. Nicotine 22-30 tumor necrosis factor Homo sapiens 109-118 22209221-7 2012 RESULTS: Pretreatment with nicotine caused a significant 2.5-fold inhibition of TNF-alpha-stimulated hBD-2 mRNA expression compared to TNF-alpha alone (p = 0.004). Nicotine 27-35 tumor necrosis factor Homo sapiens 80-89 22209221-7 2012 RESULTS: Pretreatment with nicotine caused a significant 2.5-fold inhibition of TNF-alpha-stimulated hBD-2 mRNA expression compared to TNF-alpha alone (p = 0.004). Nicotine 27-35 tumor necrosis factor Homo sapiens 135-144 22209221-8 2012 Simultaneous treatment with TNF-alpha and nicotine caused a significant 2-fold inhibition of hBD-2 mRNA compared to TNF-alpha alone (p = 0.041). Nicotine 42-50 tumor necrosis factor Homo sapiens 116-125 22209221-9 2012 CONCLUSION: The present results suggest that the pre-exposition to nicotine seems to reduce a stimulating effect of TNF-alpha on the gene expression of hBD-2. Nicotine 67-75 tumor necrosis factor Homo sapiens 116-125 22095388-10 2012 Cells that were transfected with alpha7 siRNA and subsequently incubated with nicotine and LPS, exhibited a higher expression of TNF-alpha, IL-8, and IL-6 compared with non-transfected cells or alpha1 and alpha5 siRNA-transfected cells. Nicotine 78-86 tumor necrosis factor Homo sapiens 129-138 19729077-6 2009 Apigenin significantly inhibited the nicotine- and LPS-induced production of NO, PGE2, IL-1beta, TNF-alpha, IL-6, and IL-12, and the upregulation of iNOS and COX-2 in hPDL cells. Nicotine 37-45 tumor necrosis factor Homo sapiens 97-106 22425227-3 2012 Secretion of IL-12 and TNF-alpha by lipopolysaccharide (LPS)-stimulated NiDCs was significantly suppressed compared to monocyte-derived DCs grown without nicotine. Nicotine 154-162 tumor necrosis factor Homo sapiens 23-32 22441542-7 2012 RESULTS: Repeated nicotine exposure upregulated CHRNA7 expression on THP-I monocytes and led to an enhanced potential of alpha7 nAChR agonist GSK1345038A to reduce TNF levels. Nicotine 18-26 tumor necrosis factor Homo sapiens 164-167 21691078-0 2011 Nicotine reduces TNF-alpha expression through a alpha7 nAChR/MyD88/NF-kB pathway in HBE16 airway epithelial cells. Nicotine 0-8 tumor necrosis factor Homo sapiens 17-26 21691078-1 2011 AIMS: To explore the signaling mechanism associated with the inhibitory effect of nicotine on tumor necrosis factor (TNF)- alpha expression in human airway epithelial cells. Nicotine 82-90 tumor necrosis factor Homo sapiens 94-128 21691078-4 2011 The effects of nicotine on the production of proinflammatory factors TNF-alpha, in transfected cells were analyzed. Nicotine 15-23 tumor necrosis factor Homo sapiens 69-78 21691078-6 2011 RESULTS: The production of TNF-alpha was lower in cells pretreated with nicotine before lipopolysaccharide (LPS) stimulation, compared with LPS-only-treated cells. Nicotine 72-80 tumor necrosis factor Homo sapiens 27-36 21691078-7 2011 In contrast, in alpha7 siRNA-transfected cells incubated with nicotine and LPS, TNF-alpha expression was higher than that in non-transfected cells or in alpha1 or alpha5 siRNA-transfected cells. Nicotine 62-70 tumor necrosis factor Homo sapiens 80-89 21691078-11 2011 CONCLUSION: Nicotine reduces TNF-alpha expression in HBE16 airway epithelial cells, mainly through an alpha7 nAChR/MyD88/NF-kappaB pathway. Nicotine 12-20 tumor necrosis factor Homo sapiens 29-38 20665032-0 2012 Nicotine inhibits tumor necrosis factor-alpha induced IL-6 and IL-8 secretion in fibroblast-like synoviocytes from patients with rheumatoid arthritis. Nicotine 0-8 tumor necrosis factor Homo sapiens 18-45 20665032-4 2012 Nicotine at concentrations of 0.1-10 muM dose reduced the protein and mRNA expression of IL-6 and IL-8 induced by tumor necrosis factor-alpha (TNFalpha). Nicotine 0-8 tumor necrosis factor Homo sapiens 114-141 20665032-4 2012 Nicotine at concentrations of 0.1-10 muM dose reduced the protein and mRNA expression of IL-6 and IL-8 induced by tumor necrosis factor-alpha (TNFalpha). Nicotine 0-8 tumor necrosis factor Homo sapiens 143-151 20665032-6 2012 In conclusion, nicotine can inhibit the TNFalpha dependant inflammatory pathway in synoviocytes by suppressing the activation of the NF-kappaB pathway. Nicotine 15-23 tumor necrosis factor Homo sapiens 40-48 21606497-1 2011 Nicotine inhibits the release of TNF-alpha from macrophage through activation of STAT3. Nicotine 0-8 tumor necrosis factor Homo sapiens 33-42 21606497-4 2011 Nicotine induced activation of STAT3 enhanced STAT3 binding to the TTP promoter, increased TTP promoter activity, and increased TTP expression resulting in the suppression of LPS-stimulated TNF-alpha production. Nicotine 0-8 tumor necrosis factor Homo sapiens 190-199 21606497-5 2011 Overexpression of a dominant negative mutant of STAT3 (R382W) or down-regulation of STAT3 by siRNA abolished nicotine-induced TTP expression and suppression of LPS-stimulated TNF-alpha production. Nicotine 109-117 tumor necrosis factor Homo sapiens 175-184 21606497-6 2011 Nicotine enhanced the decay of TNF-alpha mRNA and decreased luciferase expression of a TNF-alpha 3"-UTR reporter plasmid in U937 cells. Nicotine 0-8 tumor necrosis factor Homo sapiens 31-40 21606497-6 2011 Nicotine enhanced the decay of TNF-alpha mRNA and decreased luciferase expression of a TNF-alpha 3"-UTR reporter plasmid in U937 cells. Nicotine 0-8 tumor necrosis factor Homo sapiens 87-96 18305393-1 2008 Recent studies have reported that the cholinergic anti-inflammatory pathway regulates peripheral inflammatory responses via alpha7 nicotinic acetylcholine receptors (alpha7 nAChRs) and that acetylcholine and nicotine regulate the expression of proinflammatory mediators such as TNF-alpha and prostaglandin E2 in microglial cultures. Nicotine 208-216 tumor necrosis factor Homo sapiens 278-287 18618634-8 2008 In all groups, nicotine reduced LPS- and PHA (0.5 microg/mL)-stimulated production of IL1beta, IL10, TGFbeta, and TNFalpha (P < 0.001). Nicotine 15-23 tumor necrosis factor Homo sapiens 114-122 18669662-6 2008 Administration of nicotine, a pharmacological agonist of alpha7, attenuated TNF immunoreactivity in these specific macrophage subpopulations. Nicotine 18-26 tumor necrosis factor Homo sapiens 76-79 16328020-13 2006 In human osteoblasts, nicotine also induced an increase in the TNF-alpha secretion and estradiol opposed this increase. Nicotine 22-30 tumor necrosis factor Homo sapiens 63-72 16980882-6 2006 In the present study, we found that nicotine suppressed the expression of CD14, toll-like receptor 4, intercellular adhesion molecule 1, B7.1, and CD40 on monocytes and the production of TNF-alpha, but not interleukin 10, in human peripheral blood mononuclear cells in the presence of LPS. Nicotine 36-44 tumor necrosis factor Homo sapiens 187-196 16980882-8 2006 Therefore, nicotine might inhibit the LPS receptor complex expression via alpha7-nAChR, thus leading to a decrease in the adhesion molecule expression and TNF-alpha production. Nicotine 11-19 tumor necrosis factor Homo sapiens 155-164 16966384-4 2006 In the present study, we found that nicotine inhibited the IL-18-enhanced expression of ICAM-1, B7.2, and CD40 on monocytes, and the production of IL-12, IFN-gamma, and TNF-alpha by PBMC. Nicotine 36-44 tumor necrosis factor Homo sapiens 169-178 16968406-5 2006 Pretreatment with low-dose nicotine caused inhibition of TNF-alpha, PGE(2), MIP-1alpha and MIP-1alpha production, and mRNA expression of TNF-alpha, MIP-1alpha and MIP-1alpha and COX-2 in lipopolysaccharide (LPS)-activated monocytes. Nicotine 27-35 tumor necrosis factor Homo sapiens 57-66 16968406-5 2006 Pretreatment with low-dose nicotine caused inhibition of TNF-alpha, PGE(2), MIP-1alpha and MIP-1alpha production, and mRNA expression of TNF-alpha, MIP-1alpha and MIP-1alpha and COX-2 in lipopolysaccharide (LPS)-activated monocytes. Nicotine 27-35 tumor necrosis factor Homo sapiens 137-146 16325875-5 2006 A likely possibility is that nicotine turns off the production of TNF-alpha by the macrophages in the lungs, rendering the patient more susceptible to the development of progressive disease from latent Mycobacterium tuberculosis infection. Nicotine 29-37 tumor necrosis factor Homo sapiens 66-75 15454119-0 2004 Nicotine could augment adhesion molecule expression in human endothelial cells through macrophages secreting TNF-alpha, IL-1beta. Nicotine 0-8 tumor necrosis factor Homo sapiens 109-118 15670336-3 2005 Nicotine and ACh have been recently reported to inhibit tumor necrosis factor-alpha (TNF-alpha) production in human macrophages as well as in mouse microglial cultures. Nicotine 0-8 tumor necrosis factor Homo sapiens 56-83 15670336-3 2005 Nicotine and ACh have been recently reported to inhibit tumor necrosis factor-alpha (TNF-alpha) production in human macrophages as well as in mouse microglial cultures. Nicotine 0-8 tumor necrosis factor Homo sapiens 85-94 15809354-6 2005 In vitro mechanistic studies revealed that nicotine blocked TNF-induced nuclear factor-kappaB nuclear entry in an inhibitor kappaB (IkappaB)alpha- and IkappaBepsilon-dependent manner. Nicotine 43-51 tumor necrosis factor Homo sapiens 60-63 15454119-7 2004 The results showed TNF-alpha, IL-1beta could reach the peak with 0.06mM nicotine treated for 24 and 12 h on Ana-1, respectively, but IL-8 and IFN-gamma had no significant alter. Nicotine 72-80 tumor necrosis factor Homo sapiens 19-28 15454119-11 2004 In conclusion, our findings suggest that nicotine could augment macrophages releasing TNF-alpha and IL-1beta, furthermore TNF-alpha and IL-1beta could up-regulate the expression of adhesion molecule and increase adhesion of monocytes to HUVECs. Nicotine 41-49 tumor necrosis factor Homo sapiens 86-95 15342104-8 2004 Furthermore, this activation, as measured by TNF-alpha and nitric oxide (NO) release, is synergistically attenuated through the alpha7 nAChR and p44/42 MAPK system by pretreatment with nicotine, and the cholinesterase inhibitor, galantamine. Nicotine 185-193 tumor necrosis factor Homo sapiens 45-54 15502843-3 2004 Nicotine, a selective cholinergic agonist, is more efficient than acetylcholine and inhibits HMGB1 release induced by either endotoxin or tumor necrosis factor-alpha (TNF-alpha). Nicotine 0-8 tumor necrosis factor Homo sapiens 138-165 15502843-3 2004 Nicotine, a selective cholinergic agonist, is more efficient than acetylcholine and inhibits HMGB1 release induced by either endotoxin or tumor necrosis factor-alpha (TNF-alpha). Nicotine 0-8 tumor necrosis factor Homo sapiens 167-176 12628462-1 2003 In the present study we have used RT-PCR to investigate nicotinic acetylcholine receptor (nAChR) subunit expression, and studied the effect of nicotine on TNFalpha-induced cytokine (IL-8) release in the epithelial cell line HT29. Nicotine 143-151 tumor necrosis factor Homo sapiens 155-163 12628462-7 2003 Nicotine significantly inhibited TNFalpha-induced IL-8 release in a concentration related manner with peak inhibition occurring at 10(-7) M (2.39 +/- 0.78 ng ml(-1), n = 5). Nicotine 0-8 tumor necrosis factor Homo sapiens 33-41 8913794-6 1996 Nicotine as well as prednisolone caused a significant inhibition of IL-2 and TNF alpha production. Nicotine 0-8 tumor necrosis factor Homo sapiens 77-86 10490998-4 1999 Neuroprotection by this cytokine requires both activation of the p55/TNF receptor type I and the release of TNF-alpha from neurons, and it is inhibited by the plant alkaloid nicotine. Nicotine 174-182 tumor necrosis factor Homo sapiens 108-117 9552164-0 1998 Nicotine blocks TNF-alpha-mediated neuroprotection to NMDA by an alpha-bungarotoxin-sensitive pathway. Nicotine 0-8 tumor necrosis factor Homo sapiens 16-25 12575320-0 2002 [Effect of nicotine on the secretion of TNF of human peripheral blood mononuclear cells in vitro]. Nicotine 11-19 tumor necrosis factor Homo sapiens 40-43 12575320-1 2002 OBJECTIVE: To observe the effect of nicotine on the secretion of TNF of human peripheral blood mononuclear cells (PBMC) in vitro, and explore the possible mechanism of the high level of TNF caused by smoking. Nicotine 36-44 tumor necrosis factor Homo sapiens 65-68 12575320-6 2002 When the concentrations of nicotine were 50 ng.ml-1 and 500 ng.ml-1, the level of TNF increased significantly in non-smokers (P < 0.05, P < 0.01). Nicotine 27-35 tumor necrosis factor Homo sapiens 82-85 12575320-7 2002 In smokers, the level of TNF significantly increased when the concentration of nicotine was 50 ng.ml-1; however, the level of TNF significantly decreased (P < 0.05), and the proliferation of PBMCs was inhibited when the concentration of nicotine was 500 ng.ml-1 (P < 0.05, P < 0.05). Nicotine 79-87 tumor necrosis factor Homo sapiens 25-28 12575320-7 2002 In smokers, the level of TNF significantly increased when the concentration of nicotine was 50 ng.ml-1; however, the level of TNF significantly decreased (P < 0.05), and the proliferation of PBMCs was inhibited when the concentration of nicotine was 500 ng.ml-1 (P < 0.05, P < 0.05). Nicotine 240-248 tumor necrosis factor Homo sapiens 25-28 12575320-7 2002 In smokers, the level of TNF significantly increased when the concentration of nicotine was 50 ng.ml-1; however, the level of TNF significantly decreased (P < 0.05), and the proliferation of PBMCs was inhibited when the concentration of nicotine was 500 ng.ml-1 (P < 0.05, P < 0.05). Nicotine 240-248 tumor necrosis factor Homo sapiens 126-129 12575320-10 2002 CONCLUSION: Nicotine can induce PBMCs to secrete more TNF, and the magnitude of the effect is strongly related to the dosage of nicotine, but a great dose of nicotine will inhibit the production of TNF. Nicotine 12-20 tumor necrosis factor Homo sapiens 54-57 12575320-10 2002 CONCLUSION: Nicotine can induce PBMCs to secrete more TNF, and the magnitude of the effect is strongly related to the dosage of nicotine, but a great dose of nicotine will inhibit the production of TNF. Nicotine 12-20 tumor necrosis factor Homo sapiens 198-201 12575320-10 2002 CONCLUSION: Nicotine can induce PBMCs to secrete more TNF, and the magnitude of the effect is strongly related to the dosage of nicotine, but a great dose of nicotine will inhibit the production of TNF. Nicotine 128-136 tumor necrosis factor Homo sapiens 54-57 12575320-10 2002 CONCLUSION: Nicotine can induce PBMCs to secrete more TNF, and the magnitude of the effect is strongly related to the dosage of nicotine, but a great dose of nicotine will inhibit the production of TNF. Nicotine 128-136 tumor necrosis factor Homo sapiens 198-201 12575320-10 2002 CONCLUSION: Nicotine can induce PBMCs to secrete more TNF, and the magnitude of the effect is strongly related to the dosage of nicotine, but a great dose of nicotine will inhibit the production of TNF. Nicotine 158-166 tumor necrosis factor Homo sapiens 54-57 12575320-10 2002 CONCLUSION: Nicotine can induce PBMCs to secrete more TNF, and the magnitude of the effect is strongly related to the dosage of nicotine, but a great dose of nicotine will inhibit the production of TNF. Nicotine 158-166 tumor necrosis factor Homo sapiens 198-201 11469915-0 2001 Nicotine induces endothelial TNF-alpha expression, which mediates growth retardation in vitro. Nicotine 0-8 tumor necrosis factor Homo sapiens 29-38 11469915-16 2001 DIA showed a threefold increase in TNF-alpha activity at 1 h and a twofold increase at 3 h. Activity returned to baseline by 24 h. Cell growth was significantly decreased in cells exposed to nicotine when compared to controls on days T(2)-T(5) (P < 0.05). Nicotine 191-199 tumor necrosis factor Homo sapiens 35-44 11469915-17 2001 In cells exposed to anti-TNF-alpha and nicotine there was inhibition of the growth retardation seen in the cells containing nicotine alone. Nicotine 124-132 tumor necrosis factor Homo sapiens 25-34 11469915-19 2001 CONCLUSION: These data demonstrate the ability of endothelial cells to secrete TNF-alpha in response to nicotine at levels found in serum after smoking and also shows that endothelial cell growth retardation as a consequence of nicotine exposure may be TNF-alpha mediated. Nicotine 104-112 tumor necrosis factor Homo sapiens 79-88 11469915-19 2001 CONCLUSION: These data demonstrate the ability of endothelial cells to secrete TNF-alpha in response to nicotine at levels found in serum after smoking and also shows that endothelial cell growth retardation as a consequence of nicotine exposure may be TNF-alpha mediated. Nicotine 228-236 tumor necrosis factor Homo sapiens 79-88 11469915-19 2001 CONCLUSION: These data demonstrate the ability of endothelial cells to secrete TNF-alpha in response to nicotine at levels found in serum after smoking and also shows that endothelial cell growth retardation as a consequence of nicotine exposure may be TNF-alpha mediated. Nicotine 228-236 tumor necrosis factor Homo sapiens 253-262 10932071-7 2000 Nicotine, at a concentration comparable with that found in the highest-tar cigarettes (200 microg/mL), suppressed the production of IL-2, IFN-gamma, and TNF-alpha by only 21% to 38%. Nicotine 0-8 tumor necrosis factor Homo sapiens 153-162 10959551-7 2000 The effect of nicotine on TNFalpha production in LPS stimulated THP-1 monocyte cells in-vitro was also determined. Nicotine 14-22 tumor necrosis factor Homo sapiens 26-34 10959551-10 2000 Nicotine also caused a significant reduction in TNFalpha release from THP-1 cells. Nicotine 0-8 tumor necrosis factor Homo sapiens 48-56 10959551-12 2000 The mechanism of action of nicotine does not involve increased corticosterone levels, but may be a consequence of a reduction in TNFalpha or leukotriene B4 production. Nicotine 27-35 tumor necrosis factor Homo sapiens 129-137 10435757-6 1999 Nicotine decreased both TNF-alpha and NO responses. Nicotine 0-8 tumor necrosis factor Homo sapiens 24-33 35289351-11 2022 In-vitro studies revealed that nicotine lowers the expression of inflammatory cytokines (TNF, IL6, IL1beta) and proteins (TRAF2, P50, P65) at 1 microg/ml in TNFalpha induced SW982 cells.Nicotine from natural sources (Brassica oleracea) has been found to be an effective anti- inflammatory compound at a low dosage. Nicotine 31-39 tumor necrosis factor Homo sapiens 157-165 7923576-1 1994 The direct effect of nicotine on the expression of receptors for the tumor necrosis factor alpha (TNF alpha) and transforming growth factor beta (TGF beta) and the internalization, intracellular distribution and stability of these growth factors in cervical cancer cell line SiHa was studied. Nicotine 21-29 tumor necrosis factor Homo sapiens 69-96 7923576-1 1994 The direct effect of nicotine on the expression of receptors for the tumor necrosis factor alpha (TNF alpha) and transforming growth factor beta (TGF beta) and the internalization, intracellular distribution and stability of these growth factors in cervical cancer cell line SiHa was studied. Nicotine 21-29 tumor necrosis factor Homo sapiens 98-107 7923576-3 1994 Nicotine at 0.1% stabilized and protected from degradation [125I]TNF alpha and [125I]TGF beta internalized by cervical cancer SiHa cell line. Nicotine 0-8 tumor necrosis factor Homo sapiens 65-74 7923576-6 1994 In the presence of nicotine, both [125I]TNF alpha and [125I]TGF beta were detected in high quantities and in a non-degraded form in the cytoplasm and chromatin during 5 days of incubation. Nicotine 19-27 tumor necrosis factor Homo sapiens 40-49 7923576-8 1994 An increased intracellular accumulation of [125I]TNF alpha and [125I]TGF beta in cells exposed to nicotine occurred without changes in expression of the cell surface receptors. Nicotine 98-106 tumor necrosis factor Homo sapiens 49-58 35289351-11 2022 In-vitro studies revealed that nicotine lowers the expression of inflammatory cytokines (TNF, IL6, IL1beta) and proteins (TRAF2, P50, P65) at 1 microg/ml in TNFalpha induced SW982 cells.Nicotine from natural sources (Brassica oleracea) has been found to be an effective anti- inflammatory compound at a low dosage. Nicotine 186-194 tumor necrosis factor Homo sapiens 157-165 35441257-8 2022 Nicotine elevated the expression of pro-inflammatory cytokines TNF-alpha, IL-1beta, IL-6, IL-8, and IL-17 and decreased the anti-inflammatory IL-10 in HGFs at 24 and 72 h. Boric acid at 100 ng/mL in the medium prevented the changes induced by nicotine alone. Nicotine 0-8 tumor necrosis factor Homo sapiens 63-72