| Name | TNFalpha |
|---|---|
| Synonyms | Cachectin; DIF; TNF; TNF alpha; TNF a; TNFA; TNFSF 2; TNFSF2… |
| Name | rotenone |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 16539850 | Chen WH, Chen Y, Cui GH: Deguelin inhibits expression of IkappaBalpha protein in Raji and U937 cells. Acta Pharmacol Sin. 2006 Apr;27(4):485-90. After treatment with tumor necrosis factor alpha (TNF-alpha) or deguelin plus TNF-alpha for 15 min, there was a substantial reduction in the amount of IkappaBalpha protein. |
1(0,0,0,1) | Details |
| 15180991 | Chen K, Thomas SR, Albano A, Murphy MP, Keaney JF Jr: Mitochondrial function is required for peroxide-induced growth factor receptor transactivation and downstream signaling. J Biol Chem. 2004 Aug 13;279(33):35079-86. Epub 2004 Jun 4. Inhibition of mitochondrial function with rotenone, antimycin A, KCN, carbonylcyanide-m-chlorophenylhydrazone, or oligomycin reproduced this effect, as did generation of mitochondrial DNA-deficient (pseudo-rho (0)) cells. |
0(0,0,0,0) | Details |
| 9655528 | Josse C, Legrand-Poels S, Piret B, Sluse F, Piette J: Impairment of the mitochondrial electron chain transport prevents NF-kappa B activation by peroxide. Free Radic Biol Med. 1998 Jul 1;25(1):104-12. In this report, we first demonstrated that inhibition of the electron transport chain by either rotenone or antimycine A gave rise to dose-dependent inhibition of NF-kappa B translocation induced by 150 microM of peroxide (H2O2). |
0(0,0,0,0) | Details |
| 11952418 | Shchepina LA, Popova EN, Pletjushkina OY, Chernyak BV: Respiration and mitochondrial membrane potential are not required for apoptosis and anti-apoptotic action of Bcl-2 in HeLa cells. Biochemistry. 2002 Feb;67(2):222-6. In the present study it was shown that apoptosis and release of cytochrome c induced by staurosporine or by tumor necrosis factor-alpha in HeLa cells were not affected by inhibitors of respiration (rotenone, myxothiazol, antimycin A) or by uncouplers (CCCP, DNP) that decrease the membrane potential at the inner mitochondrial membrane. |
0(0,0,0,0) | Details |
| 11710721 | Sambo P, Baroni SS, Luchetti M, Paroncini P, Dusi S, Orlandini G, Gabrielli A: Oxidative stress in scleroderma: maintenance of scleroderma fibroblast phenotype by the constitutive up-regulation of reactive species generation through the oxidase complex pathway. Arthritis Rheum. 2001 Nov;44(11):2653-64. This suppression was not seen with rotenone, a mitochondrial oxidase inhibitor, or allopurinol, a xanthine oxidase inhibitor. |
0(0,0,0,0) | Details |
| 12800192 | Weitsman GE, Ravid A, Liberman UA, Koren R: enhances caspase-dependent and -independent TNFalpha-induced breast cancer cell death: The role of reactive species and mitochondria. Int J Cancer. 2003 Aug 20;106(2):178-86. The effect of on DeltaPsi was mimicked by rotenone, which increased both the drop in DeltaPsi and caspase activation induced by TNFalpha. |
91(1,1,1,11) | Details |
| 11597127 | Guidarelli A, Clementi E, De Nadai C, Bersacchi R, Cantoni O: TNFalpha enhances the DNA single-strand breakage induced by the short-chain lipid hydroperoxide analogue tert-butylhydroperoxide via -dependent inhibition of complex III followed by enforced and peroxide formation. Exp Cell Res. 2001 Oct 15;270(1):56-65. The following lines of evidence suggest that the enhancing effects of TNFalpha are mediated by inhibition of complex III and by the ensuing formation of superoxides and peroxide: (a) the effects of TNFalpha were mimicked by the complex III inhibitor antimycin A; (b) the effects of TNFalpha, or antimycin A, were abolished by the complex I inhibitor rotenone, or by myxothiazol, an agent which inhibits the electron flow from the reduced to cytochrome c (1) and therefore prevents formation; (c) the effects of TNFalpha, or antimycin A, were not observed in respiration-deficient cells; and (d) the effects of TNFalpha, or antimycin A, were sensitive to catalase. |
4(0,0,0,4) | Details |
| 17356569 | Zhou F, Wu JY, Sun XL, Yao HH, Ding JH, Hu G: Iptakalim alleviates rotenone-induced degeneration of dopaminergic neurons through inhibiting microglia-mediated neuroinflammation. Neuropsychopharmacology. 2007 Dec;32(12):2570-80. Epub 2007 Mar 14. In the present study, we demonstrated that systematic administration with iptakalim (IPT), an (ATP)-sensitive potassium channel (K (ATP)) opener, could alleviate rotenone-induced degeneration of dopaminergic neurons in rat substantia nigra along with the downregulation of microglial activation and mRNA levels of tumor necrosis factor-alpha (TNF-alpha) and cyclooxygenase-2 (COX-2). |
81(1,1,1,1) | Details |
| 16679036 | Lopez-Armada MJ, Carames B, Martin MA, Cillero-Pastor B, Lires-Dean M, Fuentes-Boquete I, Arenas J, Blanco FJ: Mitochondrial activity is modulated by TNFalpha and IL-1beta in normal human chondrocyte cells. Osteoarthritis Cartilage. 2006 Oct;14(10):1011-22. Epub 2006 May 5. Finally, rotenone as well as TNFalpha and IL-1beta, reduced the content of proteoglycans in the extracellular matrix of normal cartilage. |
37(0,1,1,7) | Details |
| 16257489 | Liu X, Wu JY, Zhou F, Sun XL, Yao HH, Yang Y, Ding JH, Hu G: The regulation of rotenone-induced inflammatory factor production by ATP-sensitive potassium channel expressed in BV-2 cells. Neurosci Lett. 2006 Feb 13;394(2):131-5. Epub 2005 Oct 28. K (ATP) channel openers (KCOs) including pinacidil, diazoxide and iptakalim (Ipt) exerted beneficial effects on rotenone-induced morphological alterations of BV-2 cells, decreased tumor necrosis factor alpha (TNF-alpha) production and the expression and activity of inducible isoform of synthase (iNOS). |
31(0,1,1,1) | Details |
| 18600366 | Zhang C, Park Y, Picchi A, Potter BJ: Maturation-induces endothelial dysfunction via vascular inflammation in diabetic mice. Basic Res Cardiol. 2008 Sep;103(5):407-16. Epub 2008 Jul 3. NAD (P) H oxidase inhibitor apocynin attenuated production in db/db mice at 12 weeks of age, mitochondria respiratory chain inhibitor rotenone attenuated production at 24 weeks in db/db and Db/db mice, but the combination of apocynin and rotenone reduced production at 18 weeks for db/db and Db/db mice. We hypothesized that maturation-induced vascular inflammation produces endothelial dysfunction in type II diabetes and TNFalpha plays a key role in triggering inflammation in the development of diabetes. |
5(0,0,0,5) | Details |
| 8885334 | Miesel R, Murphy MP, Kroger H: Enhanced mitochondrial radical production in patients which rheumatoid arthritis correlates with elevated levels of tumor necrosis factor alpha in plasma. Free Radic Res. 1996 Aug;25(2):161-9. |
3(0,0,0,3) | Details |
| 8989910 | Otero G, Avila MA, Emfietzoglou D, Clerch LB, Massaro D, Notario V: Increased manganese superoxide dismutase activity, protein, and mRNA levels and concurrent induction of tumor necrosis factor alpha in radiation-initiated Syrian hamster cells. Mol Carcinog. 1996 Dec;17(4):175-80. Inhibitors of (SO) anion production (thenoyltrifluoroacetone and rotenone) decreased the concentration of Mn-SOD mRNA, raising the possibility that the generation of SO radicals participated in the upregulation of Mn-SOD in cells transformed by exposure to radiation. |
2(0,0,0,2) | Details |
| 9374527 | Morales A, Garcia-Ruiz C, Miranda M, Mari M, Colell A, Ardite E, Fernandez-Checa JC: Tumor necrosis factor increases hepatocellular by transcriptional regulation of the heavy subunit chain of gamma-glutamylcysteine synthetase. J Biol Chem. 1997 Nov 28;272(48):30371-9. |
2(0,0,0,2) | Details |
| 14580847 | Dutkowski P, Krug A, Krysiak M, Dunschede F, Seifert JK, Junginger T: Detection of mitochondrial electron chain carrier redox status by transhepatic light intensity during rat liver reperfusion. Cryobiology. 2003 Oct;47(2):125-42. Mitochondrial electron chain carriers were inhibited at different sites with rotenone and in some experiments. reversed transcriptional polymerase chain reaction (RT-PCR) was performed after reperfusion concerning transcription of TNFalpha, caspase 9, and c-jun kinase (JNK). Increased formation as well as transcription of TNFalpha, caspase 9, and JNK during reperfusion after cold storage (CS) were related with completely reduced cytochromes before and during reperfusion. |
2(0,0,0,2) | Details |
| 11225736 | Li YP, Atkins CM, Sweatt JD, Reid MB: Mitochondria mediate tumor necrosis factor-alpha/NF-kappaB signaling in skeletal muscle myotubes. Antioxid Redox Signal. 1999 Spring;1(1):97-104. We found that activation of NF-kappaB by TNF-alpha was blocked by rotenone or amytal, inhibitors of complex I of the mitochondrial respiratory chain. |
2(0,0,0,2) | Details |
| 11415943 | Corda S, Laplace C, Vicaut E, Duranteau J: Rapid reactive species production by mitochondria in endothelial cells exposed to tumor necrosis factor-alpha is mediated by Am J Respir Cell Mol Biol. 2001 Jun;24(6):762-8. To determine the source of ROS, the mitochondrial respiratory chain inhibitors rotenone + thenoyltrifluoroacetone (TTFA), which inhibit electron entry to and antimycin A (AA), a blocker of were used. |
2(0,0,0,2) | Details |
| 18840762 | Eley HL, Russell ST, Tisdale MJ: Mechanism of attenuation of muscle protein degradation induced by tumor necrosis factor-alpha and angiotensin II by Am J Physiol Endocrinol Metab. 2008 Dec;295(6):E1417-26. Epub 2008 Oct 7. Formation of ROS was attenuated by rotenone, an inhibitor of the mitochondrial electron transport chain, nitro- methyl ester, an inhibitor of synthase, and SB 203580, a specific inhibitor of p38 mitogen-activated protein kinase (p38 MAPK), which also attenuated total protein degradation. |
2(0,0,0,2) | Details |
| 11229440 | Goossens V, Stange G, Moens K, Pipeleers D, Grooten J: Regulation of tumor necrosis factor-induced, mitochondria- and reactive species-dependent cell death by the electron flux through the electron transport chain complex I. Antioxid Redox Signal. 1999 Fall;1(3):285-95. |
2(0,0,0,2) | Details |
| 8662662 | Tetsuka T, Baier LD, Morrison AR: Antioxidants inhibit interleukin-1-induced cyclooxygenase and synthase expression in rat mesangial cells. J Biol Chem. 1996 May 17;271(20):11689-93. Glomerular mesangial cells produce reactive intermediates when stimulated by interleukin-1 (IL-1) or tumor necrosis factor. Another antioxidant, rotenone, which inhibits reactive intermediate production by inhibiting the mitochondrial electron transport system, did not inhibit IL-1beta-induced iNOS and Cox-2 mRNA expression but inhibited iNOS and Cox-2 protein expression, suggesting a post-transcriptional target for the inhibition of NOS and Cox-2 expression induced by IL-1beta. |
2(0,0,0,2) | Details |
| 16424801 | Lecour S, Van der Merwe E, Opie LH, Sack MN: attenuates hypoxic cell death via reactive species signaling. J Cardiovasc Pharmacol. 2006 Jan;47(1):158-63. We have previously demonstrated that tumor necrosis factor alpha (TNFalpha), a cytokine known to be induced by ischemia, independently promotes preconditioning in part via generation. Incubation of with cyclooxygenase-2 inhibitor, NS 398 (10 microM), or with a mitochondrial respiratory chain inhibitor, rotenone (10 microM) reduced the cytoprotective effect of in parallel with a partial diminution in ROS generation. |
2(0,0,0,2) | Details |
| 10554331 | Hakoda S, Ishikura H, Takeyama N, Tanaka T: Tumor necrosis factor-alpha plus actinomycin D-induced apoptosis of L929 cells is prevented by Surg Today. 1999;29(10):1059-67. Because the inhibition of mitochondrial respiration by rotenone or antimycin A suppressed the increased oxidation of both dihydrorhodamine 123 and hydroethidine, it was suggested that TNF-alpha accelerated the leakage of reactive intermediates from the mitochondrial electron transport system. |
2(0,0,0,2) | Details |
| 15530876 | Ling Z, Chang QA, Tong CW, Leurgans SE, Lipton JW, Carvey PM: Rotenone potentiates neuron loss in animals exposed to lipopolysaccharide prenatally. Exp Neurol. 2004 Dec;190(2):373-83. This DA neuron loss was long-lived and associated with permanent increases in the pro-inflammatory cytokine tumor necrosis factor alpha (TNFalpha). |
2(0,0,0,2) | Details |
| 8579111 | Bour ES, Ward LK, Cornman GA, Isom HC: Tumor necrosis factor-alpha-induced apoptosis in hepatocytes in long-term culture. Am J Pathol. 1996 Feb;148(2):485-95. |
2(0,0,0,2) | Details |
| 15650392 | Bundy RE, Hoare GS, Kite A, Beach J, Yacoub M, Marczin N: Redox regulation of p38 MAPK activation and expression of ICAM-1 and heme oxygenase-1 in human alveolar epithelial (A549) cells. Antioxid Redox Signal. 2005 Jan-Feb;7(1-2):14-24. Tumor necrosis factor-alpha (TNFalpha) and peroxide (H2O2) both activated p38, but only TNFalpha activated nuclear factor-kappaB (NF-kappaB). The mitochondrial complex I and III inhibitors, rotenone and antimycin A, and allopurinol partially inhibited H2O2- but not TNFalpha-induced p38 activation. |
2(0,0,0,2) | Details |
| 12615666 | Ungvari Z, Csiszar A, Edwards JG, Kaminski PM, Wolin MS, Kaley G, Koller A: Increased production in coronary arteries in hyperhomocysteinemia: role of tumor necrosis factor-alpha, NAD (P) H oxidase, and inducible synthase. Arterioscler Thromb Vasc Biol. 2003 Mar 1;23(3):418-24. Epub 2003 Feb 13. METHODS AND RESULTS: The increased generation of O2*- by HHcy coronary arteries was inhibited by SOD, diphenyleneiodonium, apocynin, and apocynin plus amino but was unaffected by allopurinol and rotenone. |
2(0,0,0,2) | Details |
| 17471172 | Xi L, Qian Z, Xu G, Zhou C, Sun S: Crocetin attenuates -induced insulin insensitivity and disordered tumor necrosis factor-alpha and adiponectin expression in rat adipocytes. Br J Pharmacol. 2007 Jul;151(5):610-7. Epub 2007 Apr 30. EXPERIMENTAL APPROACH: We used to induce insulin resistance in freshly isolated rat adipocytes, and observed the effect of crocetin, diphenyleneiodonium, rotenone and |
2(0,0,0,2) | Details |
| 7629499 | Zamzami N, Marchetti P, Castedo M, Decaudin D, Macho A, Hirsch T, Susin SA, Petit PX, Mignotte B, Kroemer G: Sequential reduction of mitochondrial transmembrane potential and generation of reactive species in early programmed cell death. J Exp Med. 1995 Aug 1;182(2):367-77. This sequence of alterations accompanying early PCD is found in very different models of apoptosis induction: glucocorticoid-induced death of lymphocytes, activation-induced PCD of T cell hybridomas, and tumor necrosis factor-induced death of U937 cells. This step can be selectively inhibited by rotenone and ruthenium red yet is not affected by cyclosporin A. |
1(0,0,0,1) | Details |
| 16413574 | Zhang C, Hein TW, Wang W, Ren Y, Shipley RD, Kuo L: Activation of JNK and xanthine oxidase by TNF-alpha impairs -mediated dilation of coronary arterioles. J Mol Cell Cardiol. 2006 Feb;40(2):247-57. Epub 2006 Jan 18. Conversely, the effects of TNF were insensitive to inhibitors of p38 (SB203580), ERK (PD98059), NAD (P) H oxidase (apocynin), or mitochondrial respiratory chain (rotenone). Elevated levels of tumor necrosis factor-alpha (TNF), a proinflammatory cytokine, are associated with coronary artery disease. |
1(0,0,0,1) | Details |
| 16952909 | Dell'Eva R, Ambrosini C, Minghelli S, Noonan DM, Albini A, Ferrari N: The Akt inhibitor deguelin, is an angiopreventive agent also acting on the NF-kappaB pathway. Carcinogenesis. 2007 Feb;28(2):404-13. Epub 2006 Sep 4. In addition to Akt, the nuclear factor-kappaB (NF-kappaB) kinase pathway, which plays a critical role in the regulation of inflammation, vascular homeostasis and angiogenesis, was also repressed by deguelin even in the presence of inflammatory stimuli such as tumor necrosis factor-alpha (TNF-alpha). |
1(0,0,0,1) | Details |
| 10973919 | Deshpande SS, Angkeow P, Huang J, Ozaki M, Irani K: Rac1 inhibits TNF-alpha-induced endothelial cell apoptosis: dual regulation by reactive species. FASEB J. 2000 Sep;14(12):1705-14. Rotenone, a mitochondrial electron transport chain inhibitor, suppressed TNF-induced mitochondrial ROS production, proteolytic cleavage of procaspase-3, and apoptosis. Reactive species (ROS) have been implicated as mediators of tumor necrosis factor-alpha (TNF) -induced apoptosis. |
1(0,0,0,1) | Details |
| 17765224 | Yang D, Elner SG, Bian ZM, Till GO, Petty HR, Elner VM: Pro-inflammatory cytokines increase reactive species through mitochondria and oxidase in cultured RPE cells. Exp Eye Res. 2007 Oct;85(4):462-72. Epub 2007 Jun 27. We investigated if pro-inflammatory cytokines, tumor necrosis factor (TNF)-alpha, interleukin-1 beta (IL-1 beta), and interferon-gamma (IFN-gamma), induce ROS in human retinal pigment epithelial (RPE) cells. Thenoyltrifluoroacetone (TTFA), an inhibitor of mitochondrial respiratory chain, blocked TNF-alpha- and IFN-gamma-, but not IL-1 beta-induced ROS, whereas other two mitochondrial respiratory chain inhibitors, rotenone and antimycin A, had no effect. |
1(0,0,0,1) | Details |
| 12065751 | Waldmeier PC, Feldtrauer JJ, Qian T, Lemasters JJ: Inhibition of the mitochondrial permeability transition by the nonimmunosuppressive cyclosporin derivative NIM811. Mol Pharmacol. 2002 Jul;62(1):22-9. Using two newly developed microtiter plate assays, one measuring mitochondrial swelling from absorbance and the other measuring mitochondrial membrane potential from changes in safranin fluorescence, we show that NIM811 blocks the MPT induced by and inorganic alone or in combination with the dopaminergic neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, the complex I inhibitor rotenone, and the prooxidant t-butylhydroperoxide. Additionally, we show that NIM811 blocks cell killing and prevents in situ mitochondrial inner membrane permeabilization and depolarization during tumor necrosis factor-alpha-induced apoptosis to cultured rat hepatocytes. |
1(0,0,0,1) | Details |
| 16647052 | Muzaffar S, Shukla N, Angelini GD, Jeremy JY: auto-augments formation and upregulates gp91 (phox) expression in porcine pulmonary artery endothelial cells: inhibition by iloprost. Eur J Pharmacol. 2006 May 24;538(1-3):108-14. Epub 2006 Mar 28. Rotenone and allopurinol were without effect. Pulmonary artery endothelial cells were incubated with /xanthine oxidase which generates or tumour necrosis factor alpha (TNFalpha) or A (2) analogue, U46619 (+/- superoxide dismutase [SOD] or catalase or iloprost) for 16 h. |
1(0,0,0,1) | Details |
| 7532384 | Duval DL, Sieg DJ, Billings RE: Regulation of hepatic synthase by reactive intermediates and Arch Biochem Biophys. 1995 Feb 1;316(2):699-706. synthase (NOS) induction by tumor necrosis factor-alpha (TNF alpha) is synergized by interferon-gamma, and both NOS activity and gene expression are maximal by 10 h and maintained through 24 h. NOS induction in TNF alpha-treated cells is reduced by rotenone, a mitochondrial complex 1 inhibitor. |
1(0,0,0,1) | Details |
| 8760145 | Warner BB, Stuart L, Gebb S, Wispe JR: Redox regulation of manganese superoxide dismutase. . Am J Physiol. 1996 Jul;271(1 Pt 1):L150-8. In this study, we tested the hypothesis that ROS are directly involved in the induction of the mitochondrial antioxidant manganese superoxide dismutase (MnSOD) and mediate the induction of MnSOD by tumor necrosis factor-alpha (TNF-alpha). |
1(0,0,0,1) | Details |
| 8700134 | Duval DL, Miller DR, Collier J, Billings RE: Characterization of hepatic synthase: identification as the cytokine-inducible form primarily regulated by oxidants. Mol Pharmacol. 1996 Aug;50(2):277-84. Cytokine treatment increased nuclear factor-kappa B binding, and the addition of antioxidants or rotenone inhibited cytokine activation. Induction of hepatic synthase (NOS) by tumor necrosis factor-alpha (TNF alpha), interleukin-1 beta (IL-1 beta), interferon-gamma (IFN gamma), interleukin-6 (IL-6), and lipopolysaccharide was assessed as activity and immunoreactive protein. |
1(0,0,0,1) | Details |
| 17520785 | Yi PL, Tsai CH, Lu MK, Liu HJ, Chen YC, Chang FC: Interleukin-1beta mediates sleep alteration in rats with rotenone-induced parkinsonism. Sleep. 2007 Apr 1;30(4):413-25. Protein expression of cytokines, ie, IL-1beta and tumor necrosis factor alpha (TNF-alpha), in 5 distinct brain regions was also determined by Western blot and enzyme-linked immunosorbent assay (ELISA). |
1(0,0,0,1) | Details |
| 8445326 | Tucker SD, Auzenne EJ, Sivaramakrishnan MR: Inhibition of tumor cell mitochondrial respiration by macrophage cytotoxic mediators distinct from interferon-gamma. J Leukoc Biol. 1993 Feb;53(2):138-43. Macrophage-mediated inhibition of mitochondrial respiration in EMT-6 murine mammary adenocarcinoma cells can be mimicked in vitro by treatment of the cells with interferon-gamma (IFN-gamma) in combination with tumor necrosis factor, interleukin-1, or lipopolysaccharide. |
1(0,0,0,1) | Details |
| 18218673 | Jin S, Ray RM, Johnson LR: TNF-alpha/cycloheximide-induced apoptosis in intestinal epithelial cells requires Rac1-regulated reactive species. Am J Physiol Gastrointest Liver Physiol. 2008 Apr;294(4):G928-37. Epub 2008 Jan 24. Previously we have shown that both Rac1 and c-Jun NH (2)-terminal kinase (JNK1/2) are key proapoptotic molecules in tumor necrosis factor (TNF)-alpha/cycloheximide (CHX)-induced apoptosis in intestinal epithelial cells, whereas the role of reactive species (ROS) in apoptosis is unclear. The antioxidant, (NAC), or rotenone (Rot), the mitochondrial electron transport chain inhibitor, attenuated mitochondrial ROS production and apoptosis. |
1(0,0,0,1) | Details |