PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 31395340-2 2019 Our results demonstrated that Verapamil reduced LPS-induced pathological damage of the lung tissue, infiltration of inflammatory cells and the production of IL-1beta, TNF-alpha, and MCP-1 in the serum. Verapamil 30-39 tumor necrosis factor Mus musculus 167-176 2925281-6 1989 However, whereas verapamil, a calcium antagonist known to reverse multidrug-resistance, rendered resistant cells more sensitive to chemotherapeutic drugs, it protected the cells from killing by TNF, suggesting that drug resistance and TNF resistance may not be directly connected. Verapamil 17-26 tumor necrosis factor Mus musculus 235-238 2465008-4 1989 Pretreatment of galactosamine/TNF-alpha-injured mice with 800 mg/kg uridine or with 6 mg/kg calmidazolium fully protected the animals, while administration of either verapamil or nifedipine (100 mg/kg, respectively) had no significant effect. Verapamil 166-175 tumor necrosis factor Mus musculus 30-39 2925281-6 1989 However, whereas verapamil, a calcium antagonist known to reverse multidrug-resistance, rendered resistant cells more sensitive to chemotherapeutic drugs, it protected the cells from killing by TNF, suggesting that drug resistance and TNF resistance may not be directly connected. Verapamil 17-26 tumor necrosis factor Mus musculus 194-197 27438468-0 2016 Chronic Calcium Channel Inhibitor Verapamil Antagonizes TNF-alpha-Mediated Inflammatory Reaction and Protects Against Inflammatory Arthritis in Mice. Verapamil 34-43 tumor necrosis factor Mus musculus 56-65 30203559-6 2019 Both verapamil and nifedipine, L-VDCC inhibitors, abolished this increased contraction induced by TNF-alpha or IL-8 pretreatment. Verapamil 5-14 tumor necrosis factor Mus musculus 98-107 30203559-7 2019 Moreover, TNF-alpha treatment enhanced carbachol-induced Ca2+ influx in ASM cells, and this effect was abrogated by verapamil. Verapamil 116-125 tumor necrosis factor Mus musculus 10-19 27438468-4 2016 To investigate the role of verapamil in antagonizing TNF-alpha-mediated inflammation reaction and the underlying mechanisms, bone marrow-derived macrophages (BMDM) cells were cultured with stimulation of TNF-alpha, in the presence or absence of verapamil. Verapamil 27-36 tumor necrosis factor Mus musculus 53-62 27438468-8 2016 In addition, activity of NF-kB signaling pathway was determined both in vitro and in mice arthritis models, and verapamil inhibited TNF-alpha-induced activation of NF-kB signaling both in vitro and in mice models. Verapamil 112-121 tumor necrosis factor Mus musculus 132-141 17466955-9 2007 The enhanced TNF-alpha expression in nNOS(-/-) cardiomyocytes was abrogated by an L-type calcium channel blocker verapamil or ERK1 siRNA. Verapamil 113-122 tumor necrosis factor Mus musculus 13-22 19291858-5 2009 When given as a single agent, R(+)-verapamil significantly decreased serum levels of TNF-alpha and IFN-gamma and protected mice from endotoxin lethality. Verapamil 30-44 tumor necrosis factor Mus musculus 85-94 19291858-9 2009 The most striking differences observed between saline and R(+)-verapamil pretreated animals on combination therapy included down-regulation of TNF-alpha, higher levels of IL-6, and decreased IFN-gamma concentrations. Verapamil 58-72 tumor necrosis factor Mus musculus 143-152 12188028-0 2002 Preventive effects of a verapamil against tumor necrosis factor-alpha-induced shock symptoms: approached from lipoprotein metabolic disorders. Verapamil 24-33 tumor necrosis factor Mus musculus 42-63 10675538-0 2000 Tumor necrosis factor-induced lethal hepatitis: pharmacological intervention with verapamil, tannic acid, picotamide and K76COOH. Verapamil 82-91 tumor necrosis factor Mus musculus 0-21 12188028-1 2002 We examined the role of intracellular Ca2+ in the mechanism of the preventive effects of the Ca2+-channel blocker verapamil against lipoprotein disturbances during tumor necrosis factor (TNFa)-induced shock syndrome. Verapamil 114-123 tumor necrosis factor Mus musculus 164-185 12188028-1 2002 We examined the role of intracellular Ca2+ in the mechanism of the preventive effects of the Ca2+-channel blocker verapamil against lipoprotein disturbances during tumor necrosis factor (TNFa)-induced shock syndrome. Verapamil 114-123 tumor necrosis factor Mus musculus 187-191 12188028-4 2002 In mice treated with verapamil (10 mg/kg, s.c.), the activity of LPL 4 h after TNFalpha injection was significantly higher than in mice treated with TNFalpha alone. Verapamil 21-30 tumor necrosis factor Mus musculus 79-87 12188028-4 2002 In mice treated with verapamil (10 mg/kg, s.c.), the activity of LPL 4 h after TNFalpha injection was significantly higher than in mice treated with TNFalpha alone. Verapamil 21-30 tumor necrosis factor Mus musculus 149-157 12188028-6 2002 The administration of verapamil clearly prevented the lipoprotein damage arising from TNFalpha challenge. Verapamil 22-31 tumor necrosis factor Mus musculus 86-94 12188028-7 2002 We investigated whether verapamil could suppress TNFalpha generation in endotoxin-treated J774A.1 cells. Verapamil 24-33 tumor necrosis factor Mus musculus 49-57 12188028-8 2002 Treatment with verapamil (30 microM) markedly inhibited endotoxin (1 microg/ml)-induced TNFalpha production in these cells. Verapamil 15-24 tumor necrosis factor Mus musculus 88-96 12188028-10 2002 Verapamil may, therefore, protect against some of the various disturbances caused by changes in Ca2+ mobilization through its ability to inhibit TNFalpha production in septic shock. Verapamil 0-9 tumor necrosis factor Mus musculus 145-153 10675538-4 2000 Verapamil, a calcium-channel blocker, tannic acid, picotamide, a thromboxane A(2) receptor antagonist, and K76COOH, an inhibitor, amongst others, of complement, protected significantly against induction of lethality, release of the liver-specific enzyme alanine aminotransferase (ALT) and induction of apoptosis in the liver after TNF/GalN, except for K76COOH, which paradoxically increased ALT values after challenge, and which also protected against TNF/GalN in complement-deficient mice. Verapamil 0-9 tumor necrosis factor Mus musculus 331-334 10675538-4 2000 Verapamil, a calcium-channel blocker, tannic acid, picotamide, a thromboxane A(2) receptor antagonist, and K76COOH, an inhibitor, amongst others, of complement, protected significantly against induction of lethality, release of the liver-specific enzyme alanine aminotransferase (ALT) and induction of apoptosis in the liver after TNF/GalN, except for K76COOH, which paradoxically increased ALT values after challenge, and which also protected against TNF/GalN in complement-deficient mice. Verapamil 0-9 tumor necrosis factor Mus musculus 452-455 8858023-8 1996 RESULTS: Treatment with verapamil, TMB-8, U73122, or W7 markedly inhibited TNF release by LPSa, but had little effect on IL-1 release. Verapamil 24-33 tumor necrosis factor Mus musculus 75-78 9110418-3 1997 LPS-induced interleukin-10 plasma levels were significantly enhanced, and circulating tumor necrosis factor-alpha concentrations were significantly suppressed in animals pretreated intraperitoneally with verapamil (10 mg/kg) or diltiazem (20 mg/kg). Verapamil 204-213 tumor necrosis factor Mus musculus 86-113 10072717-7 1999 Verapamil treatment reduced the expression of cardiac NOS2 protein and the mRNAs for NOS2, TNF-alpha, and IL-1beta. Verapamil 0-9 tumor necrosis factor Mus musculus 91-100 9667821-5 1998 Previously we have demonstrated that the calcium channel blockers verapamil and diltiazem, as well as dantrolene, an agent that blocks the release of calcium from its cytoplasmic stores, inhibits tumor necrosis factor-a (TNF-alpha) and augments interleukin-10 (IL-10) plasma levels in endotoxemic BALB/c mice. Verapamil 66-75 tumor necrosis factor Mus musculus 221-230 8978594-8 1997 Calcium channel blockers, verapamil and diltiazem, could alleviate both the TNF-mediated 45Ca2+-uptake and killing activity. Verapamil 26-35 tumor necrosis factor Mus musculus 76-79