PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 31561455-4 2019 Capsaicin-induced IL-1beta, COX-2, IL-6, caspase-1, and NGF upregulation on day 3 and 7, while NALP1 and TNF-alpha upregulation was observed on day 7. Capsaicin 0-9 tumor necrosis factor Rattus norvegicus 105-114 8994052-1 1997 The capacity of the proinflammatory cytokines, tumor necrosis factor alpha (TNF alpha) and interleukin 1 beta (IL-1 beta), to modulate the sensitivity of isolated sensory neurons grown in culture to the excitatory chemical agent capsaicin was examined. Capsaicin 229-238 tumor necrosis factor Rattus norvegicus 47-74 8994052-3 1997 A 24 hr pretreatment of the neuronal cultures with TNF alpha (10 or 50 ng/ml), but not IL-1 beta (10 or 50 ng/ml), produced a concentration-dependent increase in the number of cobalt-labeled neurons after exposure to 100 nM capsaicin. Capsaicin 224-233 tumor necrosis factor Rattus norvegicus 51-60 8994052-5 1997 Similarly, pretreatment with TNF alpha (10 ng/ml for 4, 12, and 24 hr) produced a greater than twofold increase in the average peak amplitude of the inward current evoked by 100 nM capsaicin. Capsaicin 181-190 tumor necrosis factor Rattus norvegicus 29-38 8994052-8 1997 These results indicate that TNF alpha can enhance the sensitivity of sensory neurons to the excitation produced by capsaicin and that this enhancement likely is mediated by the neuronal production of prostaglandins. Capsaicin 115-124 tumor necrosis factor Rattus norvegicus 28-37 8608789-0 1995 Tumor necrosis factor-alpha prevents interleukin-1 beta from augmenting capsaicin-induced vasodilatation in the rat skin. Capsaicin 72-81 tumor necrosis factor Rattus norvegicus 0-27 8608789-1 1995 The effect of tumor necrosis factor-alpha (TNF alpha) and tumor necrosis factor-beta (TNF beta) on the capsaicin-induced increase in cutaneous blood flow was investigated in anaesthetized rats. Capsaicin 103-112 tumor necrosis factor Rattus norvegicus 14-41 8608789-5 1995 This enhancement of the cutaneous hyperaemic response to capsaicin was absent when interleukin-1 beta (50 pg) was co-injected with TNF alpha (500 pg or 5000 pg). Capsaicin 57-66 tumor necrosis factor Rattus norvegicus 131-140 32086614-11 2020 In addition, stimulating either iWAT or retroperitoneal WAT with capsaicin increased TNF-alpha or IL-1beta levels in the PVN, but the injection of capsaicin into the jugular vein, skeletal muscle, and skin had no effects on TNF-alpha or IL-1beta levels in the PVN. Capsaicin 65-74 tumor necrosis factor Rattus norvegicus 85-94 32086614-11 2020 In addition, stimulating either iWAT or retroperitoneal WAT with capsaicin increased TNF-alpha or IL-1beta levels in the PVN, but the injection of capsaicin into the jugular vein, skeletal muscle, and skin had no effects on TNF-alpha or IL-1beta levels in the PVN. Capsaicin 65-74 tumor necrosis factor Rattus norvegicus 224-233 30374312-7 2018 As TNF-alpha synthesis suppressor pentoxifylline (PTX) was previously administered into the hindlimb with femoral artery occlusion, sympathetic, and pressor responses induced by capsaicin and AITC were attenuated. Capsaicin 178-187 tumor necrosis factor Rattus norvegicus 3-12 28522561-3 2017 First, a brief pretreatment with a low dose of TNFalpha (1.44 nM, 9 min) enhanced the sensitivity of transient receptor potential vanilloid type 1 (TRPV1) receptors in these neurons in two distinct phases: the inward current evoked by capsaicin was amplified (Delta = 247%) immediately following the TNFalpha pretreatment, which gradually declined toward control and then increased again reaching another peak (Delta = 384%) after 60-90 min. Capsaicin 235-244 tumor necrosis factor Rattus norvegicus 47-55 26175075-8 2015 The pivotal role of TNF-alpha in neurogenic inflammation was further supported by the findings that incubation DRG with TNF-alpha mimicked the increased excitability of DRG neurons induced by capsaicin injection, and that TNF-alpha application enhanced cutaneous vasodilation in the hind paws induced by antidromic electrical stimulation of dorsal roots. Capsaicin 192-201 tumor necrosis factor Rattus norvegicus 20-29 26175075-8 2015 The pivotal role of TNF-alpha in neurogenic inflammation was further supported by the findings that incubation DRG with TNF-alpha mimicked the increased excitability of DRG neurons induced by capsaicin injection, and that TNF-alpha application enhanced cutaneous vasodilation in the hind paws induced by antidromic electrical stimulation of dorsal roots. Capsaicin 192-201 tumor necrosis factor Rattus norvegicus 120-129 26175075-8 2015 The pivotal role of TNF-alpha in neurogenic inflammation was further supported by the findings that incubation DRG with TNF-alpha mimicked the increased excitability of DRG neurons induced by capsaicin injection, and that TNF-alpha application enhanced cutaneous vasodilation in the hind paws induced by antidromic electrical stimulation of dorsal roots. Capsaicin 192-201 tumor necrosis factor Rattus norvegicus 120-129 15579495-8 2005 In the capsaicin group, chronic treatment with compound 48/80 restored the TNF-alpha levels to control values and prevented the neutrophil influx in BAL fluid. Capsaicin 7-16 tumor necrosis factor Rattus norvegicus 75-84 15579495-10 2005 In conclusion, chronic neuropeptide depletion promoted by neonatal capsaicin treatment up-regulates airways mast cells, which upon activation by antigen at adult ages, release large amounts of cytokines such as TNF-alpha and CINC-3 that accounts for the massive airways neutrophil infiltration. Capsaicin 67-76 tumor necrosis factor Rattus norvegicus 211-220 15082877-10 2004 Capsaicin-induced ablation of sensory neurons significantly delayed ulcer healing and this was accompanied by the significant fall in the GBF and the significant rise in the gastric mucosal gene expression of IL-1beta and TNF-alpha. Capsaicin 0-9 tumor necrosis factor Rattus norvegicus 222-231 20639352-5 2010 1) A pretreatment with TNFalpha (50 ng/ml) for ~24 h increased significantly the peak Delta[Ca(2+)](i) evoked by capsaicin (Cap) in these neurons. Capsaicin 113-122 tumor necrosis factor Rattus norvegicus 23-31 20639352-5 2010 1) A pretreatment with TNFalpha (50 ng/ml) for ~24 h increased significantly the peak Delta[Ca(2+)](i) evoked by capsaicin (Cap) in these neurons. Capsaicin 124-127 tumor necrosis factor Rattus norvegicus 23-31 19818386-0 2010 Sensitization of voltage activated calcium channel currents for capsaicin in nociceptive neurons by tumor-necrosis-factor-alpha. Capsaicin 64-73 tumor necrosis factor Rattus norvegicus 100-127 19818386-2 2010 This study examines whether TNF-alpha modulates the capsaicin-induced effects after transient receptor potential vanilloid (TRPV)-1 receptor activation on voltage activated calcium channel currents (I(Ca(V))). Capsaicin 52-61 tumor necrosis factor Rattus norvegicus 28-37 19818386-4 2010 Eliciting I(Ca(V)) in DRG neurons of rats by a depolarization from the resting potential to 0 mV, TNF-alpha (100 ng/ml) reduces I(Ca(V)) by 16.9+/-2.2%, while capsaicin (0.1 microM) decreases currents by 27+/-4.3%. Capsaicin 159-168 tumor necrosis factor Rattus norvegicus 98-107 19818386-5 2010 Pre-application of TNF-alpha (100 ng/ml) for 24h results in a sensitization of I(Ca(V)) to capsaicin (0.1 microM) with a reduction of 42.8+/-4.4% mediated by TRPV-1. Capsaicin 91-100 tumor necrosis factor Rattus norvegicus 19-28 19818386-8 2010 Summarizing, TNF-alpha sensitizes nociceptive neurons for capsaicin. Capsaicin 58-67 tumor necrosis factor Rattus norvegicus 13-22 19125874-10 2009 RESULTS: Injection of tumor necrosis factor-alpha, a cytokine implicated in the pathology of acute sinusitis and allergic rhinitis, into the V2 region was shown to lower the amount of capsaicin required to stimulate neurons located in the V1 region of the ganglion. Capsaicin 184-193 tumor necrosis factor Rattus norvegicus 22-49 19125874-14 2009 CONCLUSIONS: We propose that increased levels of tumor necrosis factor-alpha, as reported during acute sinusitis and allergic rhinitis, reduces the amount of capsaicin necessary to stimulate V1 neurons that leads to cellular changes in both V1 and V2 regions. Capsaicin 158-167 tumor necrosis factor Rattus norvegicus 49-76 18582539-0 2008 Tumor necrosis factor alpha enhances the sensitivity of rat trigeminal neurons to capsaicin. Capsaicin 82-91 tumor necrosis factor Rattus norvegicus 0-27 18582539-2 2008 This study evaluated the hypothesis that TNFalpha increases the sensitivity of rat trigeminal neurons to capsaicin via two different mechanisms triggered by either brief or sustained exposure to the cytokine. Capsaicin 105-114 tumor necrosis factor Rattus norvegicus 41-49 18582539-3 2008 A brief (5 min) application of TNFalpha significantly sensitized capsaicin-evoked accumulation of intracellular calcium ([Ca2+]i) (226.4+/-37.7 nM vs. 167.5+/-31.3 nM) and increased capsaicin-evoked nocifensive behavior (78.3+/-9.7 vs. 30.9+/-3.6 s) as compared with vehicle pretreatment (P<0.01 for both). Capsaicin 65-74 tumor necrosis factor Rattus norvegicus 31-39 18582539-3 2008 A brief (5 min) application of TNFalpha significantly sensitized capsaicin-evoked accumulation of intracellular calcium ([Ca2+]i) (226.4+/-37.7 nM vs. 167.5+/-31.3 nM) and increased capsaicin-evoked nocifensive behavior (78.3+/-9.7 vs. 30.9+/-3.6 s) as compared with vehicle pretreatment (P<0.01 for both). Capsaicin 182-191 tumor necrosis factor Rattus norvegicus 31-39 18582539-5 2008 This long-term up-regulation of TRPV1 expression by TNFalpha correlated with enhancement in capsaicin-induced calcitonin gene-related peptide release (P<0.05). Capsaicin 92-101 tumor necrosis factor Rattus norvegicus 52-60 18582539-7 2008 In summary, our data demonstrate that TNFalpha directly enhances the sensitivity of rat trigeminal neurons to capsaicin via both rapid, non-genomic mechanisms as well as sustained genomic regulation in TRPV1 expression. Capsaicin 110-119 tumor necrosis factor Rattus norvegicus 38-46 18508045-0 2008 SA13353 (1-[2-(1-Adamantyl)ethyl]-1-pentyl-3-[3-(4-pyridyl)propyl]urea) inhibits TNF-alpha production through the activation of capsaicin-sensitive afferent neurons mediated via transient receptor potential vanilloid 1 in vivo. Capsaicin 128-137 tumor necrosis factor Rattus norvegicus 81-90 18508045-6 2008 The ability of SA13353 and capsaicin to inhibit LPS-induced TNF-alpha production was eliminated by sensory denervation or capsazepine pretreatment in vivo. Capsaicin 27-36 tumor necrosis factor Rattus norvegicus 60-69 18508045-9 2008 These results suggest that SA13353 inhibits TNF-alpha production through activation of capsaicin-sensitive afferent neurons mediated via TRPV1 in vivo. Capsaicin 87-96 tumor necrosis factor Rattus norvegicus 44-53 18460982-5 2008 In renal tissues exposed to ischemia/reperfusion, neutrophil infiltration, renal superoxide production, and renal tumor necrosis factor (TNF)-alpha mRNA expression were augmented, but these alterations were attenuated by the treatment with capsaicin. Capsaicin 240-249 tumor necrosis factor Rattus norvegicus 114-147 12024109-7 2002 Administration of capsaicin and CGRP significantly enhanced I/R-induced increases in hepatic levels of 6-keto-PGF(1alpha), increased hepatic-tissue blood flow after reperfusion, and inhibited the I/R-induced increase in tissue levels of both tumor necrosis factor-alpha (TNF-alpha) and myeloperoxidase. Capsaicin 18-27 tumor necrosis factor Rattus norvegicus 242-269 12024109-7 2002 Administration of capsaicin and CGRP significantly enhanced I/R-induced increases in hepatic levels of 6-keto-PGF(1alpha), increased hepatic-tissue blood flow after reperfusion, and inhibited the I/R-induced increase in tissue levels of both tumor necrosis factor-alpha (TNF-alpha) and myeloperoxidase. Capsaicin 18-27 tumor necrosis factor Rattus norvegicus 271-280