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Interaction IDMol ATypeSpeciesVerbNatureMol BTypeSpecies
14032LIFProteinHomo sapiens-eIncreases activityindirectStat1ProteinMus musculus
IFN-gamma is a potent activator of STAT 1 and a weaker activator of STAT 3, whereas LIF and OSM are potent activators of STAT 3 and weaker activators of STAT 1.
33672AlitretinoinSmall moleculeSmall moleculeDecreases expressionindirectTNFRNAHomo sapiens-e
The RXR ligand, 9-cis retinoic acid (9cRA), reduced TNF-alpha mRNA abundance in BMMs, but increased CD14 mRNA levels. 9cRA decreases TNF-alpha mRNA by destabilizing the transcript, and possibly also by forming transcriptionally inactive complex with 1 ,25(OH)(2)D(3) on the tnfVDRE.
Regulator
61858AcetylcysteineSmall moleculeSmall moleculeInhibits expressionindirectTnfProteinRattus norvegicus
NAC treatment also blocked the ischemia/reperfusion-induced expression of tumor necrosis factor and inducible nitric oxide synthase.
68364Alendronic acidSmall moleculeSmall moleculeInhibits expressionindirectTNFProteinHomo sapiens
Alendronate exhibited dose-dependent inhibition of the production of interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) by activated monocytes. The inhibitory effect of 10(-6) M alendronate on PBMC proliferation was reversed by 10 U/ml recombinant rIL-1 beta, whereas other cytokines such as IL-6, TNF-alpha, and granulocyte-macrophage colony-stimulating factor (GM-CSF) had no effect.
Regulator
69897CaffeineSmall moleculeSmall moleculeDecreases expressionindirectTnfProteinRattus norvegicus
In contrast, dietary caffeine significantly suppressed LPS-induced enhancement not only of plasma IL-1beta, IL-6, IL-10 and IFN-gamma concentrations, but also of TNF-alpha concentration.
78335CurcuminSmall moleculeSmall moleculeDecreases expressionindirectTNFProteinHomo sapiens
Regulation of pro-inflammatory cytokine expression by curcumin in hyaline membrane disease (HMD). / Curcumin produced significant inhibition of IL-1beta and IL-8 but minimal inhibition of TNFalpha expression by preterm lung inflammatory cells at 20 uM concentrations.
Disease
79535CaptoprilSmall moleculeSmall moleculeDecreases expressionindirectTNFProteinHomo sapiens
An angiotensin converting enzyme (ACE) inhibitor (captopril) and an angiotensin II type 1 (AT1) receptor antagonist (candesartan) decreased the levels of tissue factor protein and mRNA in cultured monocytes. These alterations were accompanied by a reduction in the levels of tumour necrosis factor-alpha protein and mRNA.
80170KetamineSmall moleculeSmall moleculeInhibits activityindirectTnfProteinRattus norvegicus
All animals were pretreated intraperitoneally with CAR (150 mg/kg) 16 hr before LPS stimulation. The control rats were injected LPS with 0.5 mg/kg intravenously (i.v.). The ketamine-treated rats were injected with 100 mg/kg of ketamine intramuscularly 30 min before LPS (0.5 mg/kg) i.v. injection, followed by an i.v. infusion at 0, 5, or 10 mg/kg/hr. Serum TNF-alpha, ABGs, blood glucose, and hematological studies were determined at 0, 2, and 6 hr after the LPS challenge. Serum hepatocellular enzyme levels were measured at 6 hr after the injection. / By contrast, ketamine treatment significantly attenuated the decrease in MAP and LPS-induced TNF-alpha activity.
85115AmifostineSmall moleculeSmall moleculeDecreases expressionindirectTNFProteinHomo sapiens
Moreover, we tested the ability of such antioxidant agents to reduce the serum levels of proinflammatory cytokines IL-6 and TNFalpha. / The selected antioxidant agents were: alpha lipoic acid or carboxycysteine-lysine salt, amifostine, reduced glutathione, vitamin A plus vitamin E plus Vitamin C. / Moreover, the antioxidant treatment was able to reduce serum levels of IL-6 and TNFalpha.
89789DexamethasoneSmall moleculeSmall moleculeDecreases expressionindirectTnfProteinRattus norvegicus
Both MK 801 and DEX reduced TNF production in the ipsilateral cortex of ischemic animals by 61 and 73%, respectively (P < 0.01 vs. ischemic-control).
Disease
93735AprotininSmall moleculeSmall moleculeDecreases releaseindirectTNFProteinHomo sapiens
High dose aprotinin can suppress the release of pro-inflammatory cytokines IL-1beta, IL-8 and TNF-alpha, and enhance the release of IL-10 in patients with PH after CPB.
Disease
95405BetamethasoneSmall moleculeSmall moleculeDecreases releaseindirectTnfProteinMus musculus
We have investigated the effects of betamethasone, cyclosporin, and nedocromil on MMP2 and MMP9 activities, on TNF-alpha and IL-10 release, as well as on the recruitment of inflammatory cells in the bronchoalveolar lavage (BAL) fluid after aerosol administration of lipopolysaccharide (LPS) in mice. When mice were pretreated with betamethasone (5 mg/kg, po), MMP2 and MMP9 activities, TNF-alpha in BAL fluids, and the enhanced neutrophil number of LPS-exposed mice were reduced, whereas the level of IL-10 was increased.
Disease
139226AlbuterolSmall moleculeSmall moleculeInhibits expressionindirectTNFProteinHomo sapiens
In this article, we describe the results of studies designed to determine the extent to which IL-10 contributes to the suppression of TNF-alpha generation from LPS-stimulated human monocytes evoked by 8-bromo cyclic AMP (8-Br-cAMP), rolipram, salbutamol, and prostaglandin E2 (PGE2). / LPS evoked a time- and concentration-dependent generation of TNF-alpha (t1/2 = 4.5 h; EC50 = 273 pg/mL), which was inhibited by exogenous human recombinant (h) IL-10 (IC50 = 124 pg/mL), and by rolipram (EC50 = 420 nM), 8-Br-cAMP (EC50 = 77 (microM), PGE2 (EC50 = 15 nM) and salbutamol (EC50 = 20 nM).
156199ChloroquineSmall moleculeSmall moleculeInhibits expressionindirectTNFProteinHomo sapiens
Previously, we demonstrated that the anti-inflammatory drug chloroquine (CQ) inhibited LPS-induced TNF-alpha transcription. / These findings were supported by functional data demonstrating that CQ and PD98059 interfered with TNF expression in several human and murine cell types while neither inhibitor blocked TNF production in murine RAW264.7 macrophages, a cell line that does not require MEK-ERK signaling for TNF production.
186898GadoliniumSmall moleculeSmall moleculeInhibits expressionindirectTnfProteinRattus norvegicus
Regulation of Kupffer cell TNF gene expression during experimental acute pancreatitis: the role of p38-MAPK, ERK1/2, SAPK/JNK, and NF-kappaB. / TNF and TNF-mRNA were measured in rat livers perfused with elastase. / Elastase increased TNF and upregulated TNF-mRNA in livers (P<0.03) and Kupffer cells (P<0.001). / Gadolinium inhibited elastase-induced upregulation of TNF-mRNA (P < 0.001), TNF production (P<0.001), and attenuated SAPK/JNK, as well as ERK1/2, but not p38-MAPK. Both UO126 and SB203580 significantly inhibited elastase-induced upregulation of TNF-mRNA and TNF production (P<0.001), but only UO126 inhibited activation of NF-kappaB.
Disease
192501FenofibrateSmall moleculeSmall moleculeDecreases expressionindirectTnfProteinRattus norvegicus
We examined the effect of peroxisome proliferator-activated receptor (PPAR) activators on inflammatory responses in cultured rat brain glial cells. Four PPAR-alpha activators were tested, three fibrates (WY14643, clofibrate and fenofibrate) and an arachidonic acid derivative (5,8,11,14-eicosatetraynoic acid). / PPAR-alpha activators also suppressed lipopolysaccharide-stimulated tumor necrosis factor-alpha and monocyte chemoattractant protein-1 transcription and release.
192504ClofibrateSmall moleculeSmall moleculeDecreases releaseindirectTnfProteinRattus norvegicus
We examined the effect of peroxisome proliferator-activated receptor (PPAR) activators on inflammatory responses in cultured rat brain glial cells. Four PPAR-alpha activators were tested, three fibrates (WY14643, clofibrate and fenofibrate) and an arachidonic acid derivative (5,8,11,14-eicosatetraynoic acid). / PPAR-alpha activators also suppressed lipopolysaccharide-stimulated tumor necrosis factor-alpha and monocyte chemoattractant protein-1 transcription and release.
195021Beta-LapachoneSmall moleculeSmall moleculeInhibits expressionindirectTnfProteinRattus norvegicus
beta-Lapachone, a 1,2-naphthoquinone, is a novel chemotherapeutic agent. / The authors further performed experiments to examine the molecular mechanism of beta-lapachone on LPS-induced responses in rat alveolar macrophages and to evaluate its in vivo antiinflammatory effect. / beta-Lapachone could also inhibit the production of tumor necrosis factor-alpha induced by LPS. /beta-Lapachone, a 1,2-naphthoquinone, is a novel chemotherapeutic agent.
Disease
204586Estradiol-17betaSmall moleculeSmall moleculeDecreases expressionindirectTNFProteinHomo sapiens
Estrogen modulates the hypothalamic-pituitary-adrenal and inflammatory cytokine responses to endotoxin in women. / To determine whether estrogen has similar effects in humans, we studied the cytokine and HPA responses to a low dose of endotoxin (2--3 ng/kg) in six postmenopausal women with and without transdermal E2 (0.1 mg) replacement. / Estrogen also attenuated the endotoxin-induced release of IL-6 (P = 0.02), IL-1 receptor antagonist (P = 0.003), and TNF-alpha (P = 0.04). Mean cytokine levels with and without E2 replacement peaked at 341 +/- 94 pg/mL vs. 936 +/- 620 pg/mL for IL-6, 82 +/- 14 ng/mL vs. 133 +/- 24 ng/mL for IL-1 receptor antagonist, and 77 +/- 46 pg/mL vs. 214 +/- 87 pg/mL for TNF-alpha, respectively.
216687CelecoxibSmall moleculeSmall moleculeDecreases expressionindirectTnfProteinMus musculus
Celecoxib and NS-398 enhance photodynamic therapy by increasing in vitro apoptosis and decreasing in vivo inflammatory and angiogenic factors. / Photofrin-mediated PDT combined with either celecoxib or NS-398 increased cytotoxicity and apoptosis in mouse BA mammary carcinoma cells. / Administration of celecoxib or NS-398 attenuated tissue levels of prostaglandin E2 and vascular endothelial growth factor induced by PDT in treated tumors and also decreased the expression of proinflammatory mediators interleukin-1beta and tumor necrosis factor-alpha.
Disease
218387L-GlutamineSmall moleculeSmall moleculeDecreases releaseindirectTnfProteinRattus norvegicus
Glutamine (GLN) has been shown to attenuate cytokine release from LPS-stimulated human peripheral blood mononuclear cells; however, the in vivo antiinflammatory effect of GLN in polymicrobial sepsis and ARDS is unknown. / Either 0.75 g/kg of GLN or saline placebo (SP) was administered to male rats 1 h after cecal ligation and puncture (CLP). / GLN treatment increased MKP-1 peptide expression and significantly attenuated TNF-alpha and IL-6 6 h after CLP. / The antiinflammatory effect of GLN was associated with attenuation of ARDS and mortality.
Disease
219675GlivecSmall moleculeSmall moleculeDecreases expressionindirectTNFProteinHomo sapiens
Imatinib mesylate suppresses cytokine synthesis by activated CD4 T cells of patients with chronic myelogenous leukemia. / As cytokines are required for T-cell proliferation, we investigated the effects of IM on cytokine synthesis by T cells of CML patients by assessing cytokine synthesis by activated CD4+ and CD8+ T cells in vitro. The activation of T cells in the whole blood of IM-treated patients (CML-IM) with Staphylococcus enterotoxin B resulted in significantly lower percentages of CD4+ T cells that synthesized interleukin 2 (P = 0.017), interferon-gamma (P = 0.010), and tumor necrosis factor-alpha (P = 0.009) than did the activated T cells of control subjects.
Disease
219786AspirinSmall moleculeSmall moleculeInhibits expressionindirectTNFProteinHomo sapiens
Alcoholic liver disease (ALD) is one of the most common liver diseases in the world. Increased levels of proinflammatory cytokines, including interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha), have been correlated with the patients affected by ALD. / In this study, we demonstrated that acetaldehyde, the metabolic product of ethanol, was able to induce IL-1beta and TNF-alpha production in HepG2 cells. / However, the NF-kappaB inhibitors, such as aspirin, cyclosporin A and dexamethasone, inhibited both the acetaldehyde-induced NF-kappaB activity and the induced cytokine production.
Disease
224559CimetidineSmall moleculeSmall moleculeInhibits expressionindirectTnfProteinMus musculus
To investigate the effects of cocaine on myocardial injuries and cardiac P450 expression, BALB/c mice were injected daily intraperitoneally with cocaine (30 mg/kg) or cocaine plus pretreatment of P450 inhibitors for 14 days. / Tumor necrosis factor-alpha (TNF-alpha) content and creatine phosphokinase (CPK) activity in mice hearts and serums were significantly increased after long-term treatment with cocaine. Pretreatment with the P450 inhibitor, cimetidine (Cime, 50 mg/kg) or metyrapone (Mety, 40 mg/kg) abolished or significantly attenuated the effects of cocaine on TNF-alpha and CPK activity.
421747GenisteinSmall moleculeSmall moleculeInhibits expressionindirectTNFRNAHomo sapiens-e
Tyrosine kinase inhibitors attenuate Japanese encephalitis virus-induced neurotoxicity. / PTK inhibitors, genistein, herbimycin A, and PP2, attenuated JEV-induced neurotoxicity but failed to affect JEV replication. Infection of neuron/glia cultures with JEV produced elevated levels of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta). PTK inhibitors suppressed JEV-induced TNF-alpha and IL-1beta production at the transcriptional level. Our results suggest that PTKs, especially Src-related PTK, play roles in the production of TNF-alpha and IL-1beta during JEV infection and in the induction of neuronal death in neuron/glia cultures.
Regulator
425368IndomethacinSmall moleculeSmall moleculeDecreases expressionindirectTnfProteinMus musculus
OBJECTIVE: To assess the putative involvement of NF-kappaB and pro-inflammatory cytokines in the pathogenesis of cancer cachexia and the therapeutic efficacy of indomethacin (IND) on cachexia. METHODS: Thirty young male BALB/c mice were divided randomly into five groups: A, control; B, tumor-bearing plus saline; C, tumor-bearing plus IND (0.25 mg/kg); D, tumor-bearing plus IND (0.5 mg/kg); and E, tumor-bearing plus IND (2.0 mg/kg). Colon 26 adenocarcinoma cells of murine were inoculated subcutaneously to induce cachexia. Saline and IND were given intraperitoneally daily for 7 days from the onset of cachexia to sacrifice. / Tumor-bearing caused a significant increase in serum TNF-alpha and IL-6 levels (P < 0.01). The concentration of TNF-alpha (P < 0.05) and IL-6 (P < 0.01) in tumor-bearing mice was reduced after administration of 0.5 mg/kg IND for 7 days. / Cachexia induced by colon 26 adenocarcinoma cells may be partially attributed to the enhanced TNF-alpha and IL-6 levels which is controlled by NF-kappaB. IND may inhibit the activation of NF-kappaB, decrease serum TNF-alpha and IL-6 levels and thus alleviate the cachexia.
Disease
Regulator

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