scholarly journals Tectorigenin inhibits Caco-2 human colon cells via NF-κB pathway suppression

2015 ◽  
Vol 10 (4) ◽  
pp. 948
Author(s):  
Xiao-Yu Dai ◽  
Yong-Ming Yu ◽  
Zheng-Fang Kong ◽  
Yi-Sheng Cao ◽  
Dan-Dan Huang ◽  
...  
Keyword(s):  
Human Colon ◽  
Pathological Process ◽  
Human Colon Cancer ◽  
Colon Cells ◽  
Reverse Transcription Pcr ◽  
Contagious Diseases ◽  
Tnf Α ◽  
Cytokine Tumor Necrosis Factor ◽  
Factor Α ◽  
Necrosis Factor

<p class="Abstract">Effective immunomodulator and pro-inflammatory cytokine, Tumor necrosis factor-α (TNF-α) are considered to be responsible for connecting autoimmune pathological process and contagious diseases. TNF-α stimulates the C-X-C motif chemokine 10 (CXCL10) expression that is participated in migration of tumor, metastasis, and invasion. Tectorigenin, an o-methylated isoflavone, is present as a major portion in the Iris tectorum rhizomes. In this study, we investigated the tectorigenin effects as an anticancer drug. The obtained results showed that tectorigenin hinders the invasion of human colon cancer cells (Caco-2). We used reverse transcription PCR, q-PCR and enzyme linked immunosorbent assays to test whether the tectorigenin is involved in the inhibition of TNF-α induced CXCL-10 expression in the Caco-2 cell lines. Further, we tested TNF-α induced NF-κB activity using the tectorigenin. Collective results showed that tectorigenin inhibits the CXCL10 production by using TNF-α via NF-κB inhibition.</p><p> </p>

Epinephrine inhibits endotoxin-induced IL-1β production: roles of tumor necrosis factor-α and IL-10

1997 ◽  
Vol 273 (6) ◽  
pp. R1885-R1890 ◽  
Author(s):  
Tom Van Der Poll ◽  
Stephen F. Lowry
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Ex Vivo ◽  
Systemic Infection ◽  
Tnf Α ◽  
Cytokine Tumor Necrosis Factor ◽  
Dose Dependent Decrease ◽  
Factor Α ◽  
Necrosis Factor

Epinephrine has been found to inhibit the production of the proinflammatory cytokine tumor necrosis factor (TNF)-α and to enhance the production of anti-inflammatory cytokine interleukin (IL)-10. To determine the effect of epinephrine on IL-1β production, the following experiments were performed: 1) blood obtained from subjects at 4–21 h after the start of a continuous infusion of epinephrine (30 ng ⋅ kg−1⋅ min−1) produced less IL-1β after ex vivo stimulation with lipopolysaccharide (LPS), compared with blood drawn from subjects infused with saline; 2) in whole blood in vitro, epinephrine caused a dose-dependent decrease in LPS-induced IL-1β production, which was likely mediated via adrenergic receptors; and 3) inhibition of TNF and enhancement of IL-10 both contributed to epinephrine-induced inhibition of IL-1β production. Epinephrine, either endogenously produced or administered as a component of sepsis treatment, may attenuate excessive activity of proinflammatory cytokines early in the course of systemic infection.

scholarly journals Surface engineering of porous silicon to optimise therapeutic antibody loading and release

2015 ◽  
Vol 3 (20) ◽  
pp. 4123-4133 ◽  
Author(s):  
Steven J. P. McInnes ◽  
Chris T. Turner ◽  
Sameer A. Al-Bataineh ◽  
Marta J. I. Airaghi Leccardi ◽  
Yazad Irani ◽  
...  
Keyword(s):  
Porous Silicon ◽  
Proinflammatory Cytokine ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Surface Engineering ◽  
Chronic Wounds ◽  
Tnf Α ◽  
Cytokine Tumor Necrosis Factor ◽  
Factor Α ◽  
Necrosis Factor

Infliximab antibodies released from porous silicon microparticles can sequester the proinflammatory cytokine, tumor necrosis factor-α (TNF-α), which is elevated in uveitis and non-healing chronic wounds.

LPS-induced suppression of gastric motility relieved by TNFR:Fc construct in dorsal vagal complex

2002 ◽  
Vol 283 (3) ◽  
pp. G634-G639 ◽  
Author(s):  
Gerlinda E. Hermann ◽  
C. Amy Tovar ◽  
Richard C. Rogers
Keyword(s):  
Gastric Motility ◽  
Human Immunoglobulin ◽  
Dorsal Vagal Complex ◽  
Gastric Function ◽  
Gastric Stasis ◽  
Tnf Α ◽  
Cytokine Tumor Necrosis Factor ◽  
Loss Of Appetite ◽  
Factor Α ◽  
Necrosis Factor

Our previous studies suggested that the cytokine tumor necrosis factor-α (TNF-α) may act within the neural circuitry of the medullary dorsal vagal complex (DVC) to affect changes in gastric function, such as gastric stasis, loss of appetite, nausea, and vomiting. The definitive demonstration that endogenously generated TNF-α is capable of affecting gastric function via the DVC circuitry has been impeded by the lack of an antagonist for TNF-α. The present studies used localized central nervous system applications of the TNF-adsorbant construct (TNFR:Fc; TNF-receptor linked to the Fc portion of the human immunoglobulin IgG1) to attempt to neutralize the suppressive effects of endogenously produced TNF-α. Gastric motility of thiobutabarbital-anesthetized rats was monitored after systemic administration of lipopolysaccharide (LPS) to induce TNF-α production. Continuous perfusion of the floor of the fourth ventricle with TNFR:Fc reversed the potent gastroinhibition induced by LPS, i.e., central thyrotropin-releasing hormone-induced increases in motility were not inhibited. This disinhibition of gastric stasis was not seen after intravenous administration of similar doses of TNFR:Fc nor ventricular application of the Fc fragment of human immunoglobulin. These results validate our previous studies that suggest that circulating TNF-α may act directly within the DVC to affect gastric function in a variety of pathophysiological states.

Demyelination and Neurological Sequelae in Etanercept and Infliximab Therapies: A Review of the Literature

2005 ◽  
Vol 11a (1) ◽  
pp. 6-8
Author(s):  
Vandana K. Madkan ◽  
John Y.M. Koo
Keyword(s):  
Multiple Sclerosis ◽  
Tumor Necrosis ◽  
New Drugs ◽  
Review Of The Literature ◽  
Neurological Sequelae ◽  
Tnf Α ◽  
Cytokine Tumor Necrosis Factor ◽  
Factor Α ◽  
Necrosis Factor ◽  
New Onset

Etanercept (Enbrel) and infliximab (Remicade) are two relatively new drugs, referred to as biologics, which target the cytokine tumor necrosis factor-α (TNF-α). Both are used in the treatment of psoriasis and psoriatic arthritis. Recently, there have been rare reports of demyelinating and neurological sequelae in patients while on these therapies. The authors sought to systematically review the reported cases of new-onset neurological symptoms and exacerbation of established multiple sclerosis (MS) found in the literature to determine the causality, if any, of demyelinating events by these therapies. Although these two medications may uncover latent multiple sclerosis in patients who are prone to the disease, no cause-and-effect relationship can currently be established.

scholarly journals iRhom2 and TNF: Partners or enemies?

2019 ◽  
Vol 12 (605) ◽  
pp. eaaz0444 ◽  
Author(s):  
Marina Badenes ◽  
Colin Adrain
Keyword(s):  
Hepatic Stellate Cells ◽  
Proinflammatory Cytokine ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Stellate Cells ◽  
Protective Role ◽  
Tnf Α ◽  
Cytokine Tumor Necrosis Factor ◽  
Factor Α ◽  
Necrosis Factor

iRhom2 is an essential cofactor for ADAM17, the metalloprotease that sheds both the proinflammatory cytokine tumor necrosis factor–α (TNF-α) and TNF receptors (TNFRs) from the cell surface. In this issue of Science Signaling, Sundaram et al. demonstrate a protective role for iRhom2 in promoting ADAM17-mediated shedding of TNFRs in hepatic stellate cells, which reduces TNFR signaling and liver fibrosis in response to injury.

scholarly journals Longevity-Associated Variant of BPIFB4 Mitigates Monocyte-Mediated Acquired Immune Response

2019 ◽  
Vol 74 (Supplement_1) ◽  
pp. S38-S44 ◽  
Author(s):  
Elena Ciaglia ◽  
Francesco Montella ◽  
Anna Maciag ◽  
Pasqualina Scala ◽  
Anna Ferrario ◽  
...  
Keyword(s):  
Mononuclear Cells ◽  
Therapeutic Potential ◽  
Human Monocyte ◽  
Peripheral Blood Mononuclear ◽  
Inflammatory Status ◽  
Tnf Α ◽  
Cytokine Tumor Necrosis Factor ◽  
Pkc Alpha ◽  
Factor Α ◽  
Necrosis Factor

Abstract One of the basis of exceptional longevity is the maintaining of the balance between inflammatory and anti-inflammatory networks. The monocyte-macrophages activation plays a major role in tuning the immune responses, by oscillating between patrolling-protective to inflammatory status. Longevity-associated variant (LAV) of bactericidal/permeability-increasing fold-containing family B member 4 (BPIFB4) activates calcium, PKC-alpha, and eNOS, rescuing endothelial dysfunction in aged mice and inducing revascularization. The BPIFB4’s increment in serum of healthy long-living individuals (LLIs) compared to nonhealthy ones, its therapeutic potential in improving vascular homeostasis, which depends on immune system, together with its expression in bone marrow myeloid cells, suggests that LAV-BPIFB4 may improve immune regulation. Here we show that human monocytes exposed to LAV-BPIFB4 protein increased co-stimulatory molecules in resting state and reduced pro-inflammatory cytokine tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) after activating stimuli. Accordingly, a low percentage of CD69+ activated lymphocytes are found among LAV-BPIFB4-treated peripheral blood mononuclear cells (PBMCs). Moreover, human monocyte-derived dendritic cells (DCs) generated in presence of LAV-BPIFB4 secreted higher anti-(IL-10 and TGF-β) and lower pro-inflammatory (TNF-α and IL-1β) cytokines. Accordingly, LLIs’ plasma showed higher levels of circulating IL-10 and of neutralizing IL-1 receptor antagonist (IL-1RA) compared to controls. Thus, LAV-BPIFB4 effects on myeloid compartment could represent one example of a genetic predisposition carried by LLIs to protect from immunological dysfunctions.

TNF-α-induced c-Fos generation in the nucleus of the solitary tract is blocked by NBQX and MK-801

2001 ◽  
Vol 281 (5) ◽  
pp. R1394-R1400 ◽  
Author(s):  
Gregory S. Emch ◽  
Gerlinda E. Hermann ◽  
Richard C. Rogers
Keyword(s):  
Nmda Antagonist ◽  
Early Gene ◽  
Solitary Tract ◽  
Excitatory Effect ◽  
Mk 801 ◽  
Tnf Α ◽  
Cytokine Tumor Necrosis Factor ◽  
Fos Expression ◽  
Factor Α ◽  
Necrosis Factor

Previous studies have shown that identified neurons of the nucleus of the solitary tract (NST) are excited by the cytokine tumor necrosis factor-α (TNF-α). Vagal afferent connections with the NST are predominantly glutaminergic. Therefore, we hypothesized that TNF-α effects on NST neurons may be via modulation of glutamate neurotransmission. The present study used activation of the immediate early gene product c-Fos as a marker for neuronal activation in the NST. c-Fos expression was evaluated after microinjections of TNF-α in the presence or absence of either the α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor antagonist 1,2,3,4-tetrahydro-6-nitro-2,3-dioxo-benzo[f]quinoxaline-7-sulfonamide disodium (NBQX) or the N-methyl-d- aspartate (NMDA) antagonist MK-801. To assess the specificity of the interaction between TNF-α and glutamate, c-Fos expression was also evaluated after injection of oxytocin (OT) (which has a direct excitatory effect in this area of the brain stem) in the presence and absence of NBQX or MK-801. c-Fos labeling was significantly increased in the NST after TNF-α exposure. Coinjection of either NBQX or MK-801 with TNF-α prevented significant c-Fos induction in the NST. Microinjections of OT also induced significant NST c-Fos elevation, but this expression was unaffected by coinjection of either antagonist with OT. These data lead us to conclude that TNF-α activation of NST neurons depends on glutamate and such an interaction is not generalized to all agonists that act on the NST.

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