scholarly journals Anti-allergic Inflammatory Triterpenoids Isolated from the Spikes of Prunella Vulgaris

2016 ◽  
Vol 11 (1) ◽  
pp. 1934578X1601100 ◽  
Author(s):  
Hyun Gyu Choi ◽  
Tae Hoon Kim ◽  
Sang-Hyun Kim ◽  
Jeong Ah Kim
Keyword(s):  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Inhibitory Effect ◽  
Prunella Vulgaris ◽  
Tnf Α ◽  
Factor Α ◽  
First Time ◽  
Necrosis Factor ◽  
Pro Inflammatory Cytokines ◽  
Inflammatory Effect

Twelve known triterpenoids (1–12) and two steroids (13 and 14) have been isolated from the spike of the plant Prunella vulgaris. Among them, 2α,3α,23-trihydroxyursa-12,20(30)-dien-28-oic acid (10) was isolated for the first time from this plant. All isolates were evaluated for their inhibitory effect on the gene expression of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), and release of histamine in human mast cells. β-Amyrin (5), 10, and euscaphic acid (12) showed suppression of histamine release with percentage inhibitions of 46.7, 57.9, and 54.2%, respectively. In addition, 5 and 10 showed strong inhibition of TNF-α and IL-6 in the test for pro-inflammatory cytokines. Our results suggest that compounds 5 and 10 largely contribute to the anti-allergic inflammatory effect of P. vulgaris.

scholarly journals ANTI-INFLAMMATORY EFFECT OF ELETTARIA CARDAMOM OIL ON CARRAGEENAN-INDUCED PAW EDEMA USING RATS BASED ON TUMOR NECROSIS FACTOR α, INTERLEUKIN 6, AND INTERLEUKIN 1 LEVELS IN SERUM

2018 ◽  
Vol 11 (2) ◽  
pp. 207 ◽  
Author(s):  
Nithya Sermugapandian ◽  
Rubini R ◽  
Martina V
Keyword(s):  
Tumor Necrosis Factor ◽  
Inflammatory Cytokines ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Paw Edema ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Necrosis Factor ◽  
Pro Inflammatory Cytokines ◽  
Inflammatory Effect

 Objective: In this study, we evaluated the anti-inflammatory effect of Elettaria cardamom oil and the underlying mechanism using in vivo models of inflammation.Methods: Male Sprague–Dawley rats, 4-6 weeks old, weighing 120-130 gms are used for the study. The anti-inflammatory study of E. cardamom oil was studied by injecting 0.1 ml of 1% carrageenan to the subplantar region of the right hind paw of rats. The development of acute inflammation was measured at the end of every 1st, 2nd, 3rd, 4th, 5th, and 6th h using plethysmometer.Results: As results from the above study, E. cardamom oil at a dose of 0.175 ml/kg was less significant than that of E. cardamom oil at a dose of 0.280 ml/kg when given orally. A p<0.05 shows a significant decrease in paw edema. It also reduced the levels of pro-inflammatory cytokines such as tumor necrosis factor α, interleukin (IL) 1, and IL 6 levels in the serum. The histopathology results also showed a significant reduction of congested blood vessels with no marked impression for inflammation.Conclusion: E. cardamom oil possesses anti-inflammatory activity in dose-dependent manner as they inhibit the levels of pro-inflammatory cytokines.

scholarly journals Tumor necrosis factor alpha reduces intestinal vitamin C uptake: a role for NF-κB-mediated signaling

2018 ◽  
Vol 315 (2) ◽  
pp. G241-G248 ◽  
Author(s):  
Veedamali S. Subramanian ◽  
Subrata Sabui ◽  
Ganapathy A. Subramenium ◽  
Jonathan S. Marchant ◽  
Hamid M. Said
Keyword(s):  
Tumor Necrosis Factor ◽  
Vitamin C ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Inhibitory Effect ◽  
Significant Inhibition ◽  
Tnf Α ◽  
Sodium Dependent ◽  
Factor Α ◽  
Necrosis Factor

Sodium-dependent vitamin C transporter-1 (SVCT-1) is the major transporter mediating intestinal vitamin C uptake. Intestinal inflammation and prolonged infection are associated with increased serum and intestinal mucosa levels of tumor necrosis factor-α (TNF-α), which also exerts profound effects on the intestinal absorption process. Elevated levels of TNF-α have been linked to the pathogenesis of inflammatory bowel disease (IBD) and malabsorption of nutrients, and patients with this condition have low levels of vitamin C. To date, little is known about the effect of TNF-α on intestinal absorption of vitamin C. We studied the impact of TNF-α on ascorbic acid (AA) transport using a variety of intestinal preparations. The expression level of human SVCT-1 mRNA is significantly lower in patients with IBD. TNF-α treated Caco-2 cells and mice showed a significant inhibition of intestinal14C-AA uptake. This inhibition was associated with significant decreases in SVCT-1 protein, mRNA, and heterogeneous nuclear RNA levels in TNF-α treated Caco-2 cells, mouse jejunum, and enteroids. Also, TNF-α caused a significant inhibition in the SLC23A1 promoter activity. Furthermore, treatment of Caco-2 cells with celastrol (NF-κB inhibitor) blocked the inhibitory effect caused by TNF-α on AA uptake, SVCT-1 protein, and mRNA expression, as well as the activity of SLC23A1 promoter. Treatment of TNF-α also led to a significant decrease in the expression of hepatocyte nuclear factor-1-α, which drives the basal activity of SLC23A1 promoter, and this effect was reversed by celastrol. Together, these findings show that TNF-α inhibits intestinal AA uptake, and this effect is mediated, at least in part, at the level of transcription of the SLC23A1 gene via the NF-κB pathway.NEW & NOTEWORTHY Our findings show that tumor necrosis factor-α inhibits intestinal ascorbic acid uptake in both in vitro and in vivo systems, and this inhibitory effect is mediated, at least in part, at the level of transcription of the SLC23A1 (sodium-dependent vitamin C transporter-1) gene via the NF-κB pathway.

scholarly journals Serum PR3-ANCA Is a Predictor of Primary Nonresponse to Anti-TNF-α Agents in Patients with Ulcerative Colitis

2021 ◽  
pp. 1-6
Author(s):  
Atsushi Yoshida ◽  
Katsuyoshi Matsuoka ◽  
Fumiaki Ueno ◽  
Toshio Morizane ◽  
Yutaka Endo ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Odds Ratio ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Study Data ◽  
Mayo Score ◽  
Tnf Α ◽  
Factor Α ◽  
First Time ◽  
Necrosis Factor

<b><i>Background:</i></b> Anti-tumor necrosis factor-α (TNF-α) agents are effective for moderately to severely active ulcerative colitis (UC). Nonetheless, a proportion of patients fail to respond to these agents as therapy for induction of remission. Recent studies indicated that perinuclear anti-neutrophil cytoplasmic antibody (p-ANCA) may predict response to anti-TNF-α agents in UC patients. However, whether PR3-ANCA can predict primary nonresponse (PNR) to anti-TNF-α agents has not yet been evaluated. The aim of this study was to examine whether PR3-ANCA can predict PNR to anti-TNF-α in UC patients. <b><i>Methods:</i></b> This was a single-center retrospective study. Data were extracted from 50 patients with UC who had measurements of PR3-ANCA and received anti-TNF-α agents for the first time as induction therapy. The primary endpoint of this study was a proportion of patients with PNR stratified by PR3-ANCA positivity. PNR to anti-TNF-α agents was defined as failure to achieve reduction in partial Mayo score by 2 or more points and change to other therapeutics within 6 weeks. <b><i>Results:</i></b> Fourteen (28%) of the 50 patients were PR3-ANCA positive. Seventeen (34%) of the 50 patients demonstrated PNR. Eleven (78.6%) of the 14 PR3-ANCA-positive patients demonstrated PNR, while 6 (16.7%) of the 36 PR3-ANCA-negative patients demonstrated PNR. Multivariate analysis demonstrated that PR3-ANCA positivity was associated with PNR to anti-TNF-α agents (odds ratio 19.29, 95% CI: 3.30–172.67; <i>p</i> = 0.002). <b><i>Conclusion:</i></b> PR3-ANCA positivity can predict PNR to anti-TNF-α agents in UC patients.

scholarly journals Acute Erythroderma in a Patient Receiving TNF-α-Blocking Therapy for Hidradenitis Suppurativa

2018 ◽  
Vol 10 (1) ◽  
pp. 7-12 ◽  
Author(s):  
Farida Benhadou ◽  
Guillaume Hellgren ◽  
Fabienne Willaert ◽  
Véronique del Marmol
Keyword(s):  
Tumor Necrosis Factor ◽  
Inflammatory Response ◽  
Hidradenitis Suppurativa ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Tnf Α ◽  
Adalimumab Therapy ◽  
Factor Α ◽  
First Time ◽  
Necrosis Factor

Tumor necrosis factor-α (TNF-α) normally binds to TNF-α receptors, leading to the inflammatory response of autoimmune diseases. Adalimumab is a TNF-inhibiting, anti-inflammatory, biological medication which binds to TNF-α, thus reducing this inflammatory response. The use of TNF-α-inhibiting medication, such as adalimumab, being the first FDA-approved treatment for hidradenitis suppurativa, has drastically changed the management of dermatological diseases. One rarely reported manifestation that occurs as a side effect associated with the use of TNF-α-blocking agents is erythroderma. This study, for the first time, reports the case of a patient suffering from hidradenitis suppurativa with concomitant psoriasis, who developed a severe and acute erythrodermic rash after the start of adalimumab therapy.

Ginsenoside Rg3 attenuated omethoate-induced lung injury in rats

2015 ◽  
Vol 35 (6) ◽  
pp. 677-684 ◽  
Author(s):  
J Wang ◽  
XF Yu ◽  
JJ Zhao ◽  
SM Shi ◽  
L Fu ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Lung Injury ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Histopathological Examination ◽  
Ginsenoside Rg3 ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor ◽  
Inflammatory Effect

Organophosphorus exposure affects different organs such as the lung, gastrointestinal tract, liver, and brain. The present experiment aimed to evaluate the effect of ginsenoside Rg3 on lung injury induced by acute omethoate poisoning. Rats were administered with omethoate subcutaneously at a single dose of 60 mg/kg, followed by ginsenoside Rg3 (5, 10, or 20 mg/kg) treatment. Histopathological examination of the lung was performed at 24 h after the omethoate exposure. The antioxidative parameters in the lung were also assayed. Moreover, the activities of acetylcholinesterase, myeloperoxidase, and the content of tumor necrosis factor α (TNF-α) in the lung were determined. The results showed that ginsenoside Rg3 attenuated omethoate-induced lung injury. Ginsenoside Rg3 increased the level of glutathione in the lung ( p < 0.05 or p < 0.01). The altered activities of superoxide dismutase and catalase in the lung were also ameliorated by ginsenoside Rg3 treatment ( p < 0.05 or p < 0.01). Ginsenoside Rg3 caused significant reductions in the contents of malondialdehyde, TNF-α, and the activity of myeloperoxidase ( p < 0.05 or p < 0.01). The present study demonstrated that ginsenoside Rg3 had a protective effect against omethoate-induced lung injury in rats, and the mechanisms were related to its antioxidant potential and anti-inflammatory effect.

#50 Gestational exposure of tumor necrosis factor-α (TNF-α) inhibitor drugs

2019 ◽  
Vol 88 ◽  
pp. 149-150 ◽  
Author(s):  
Erkoseoglu Ilknur ◽  
Kadioglu Mine ◽  
Cavusoglu Irem ◽  
Sisman Mulkiye ◽  
Aran Turhan ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Gestational Exposure ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Tumor necrosis factor α Inhibition for Alzheimer’s Disease

2017 ◽  
Vol 9 ◽  
pp. 117957351770927 ◽  
Author(s):  
Rudy Chang ◽  
Kei-Lwun Yee ◽  
Rachita K Sumbria
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Short Review ◽  
Tnf Α ◽  
Factor Α ◽  
Ad Therapy ◽  
Necrosis Factor

Tumor necrosis factor α (TNF-α) plays a central role in the pathophysiology of Alzheimer’s disease (AD). Food and Drug Administration–approved biologic TNF-α inhibitors are thus a potential treatment for AD, but they do not cross the blood-brain barrier. In this short review, we discuss the involvement of TNF-α in AD, challenges associated with the development of existing biologic TNF-α inhibitors for AD, and potential therapeutic strategies for targeting TNF-α for AD therapy.

Tumor necrosis factor-α-associated lysosomal permeabilization is cathepsin B dependent

2002 ◽  
Vol 283 (4) ◽  
pp. G947-G956 ◽  
Author(s):  
Nathan W. Werneburg ◽  
M. Eugenia Guicciardi ◽  
Steven F. Bronk ◽  
Gregory J. Gores
Keyword(s):  
Tumor Necrosis Factor ◽  
Cathepsin B ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Fluorescent Protein ◽  
Tnf Α ◽  
Calcein Release ◽  
Green Fluorescent ◽  
Factor Α ◽  
Necrosis Factor

Cathepsin B (Cat B) is released from lysososomes during tumor necrosis factor-α (TNF-α) cytotoxic signaling in hepatocytes and contributes to cell death. Sphingosine has recently been implicated in lysosomal permeabilization and is increased in the liver by TNF-α. Thus the aims of this study were to examine the mechanisms involved in TNF-α-associated lysosomal permeabilization, especially the role of sphingosine. Confocal microscopy demonstrated Cat B-green fluorescent protein and LysoTracker Red were both released from lysosomes after treatment of McNtcp.24 cells with TNF-α/actinomycin D, a finding compatible with lysosomal destabilization. In contrast, endosomes labeled with Texas Red dextran remained intact, suggesting lysosomes were specifically targeted for permeabilization. LysoTracker Red was released from lysosomes in hepatocytes treated with TNF-α or sphingosine in Cat B(+/+) but not Cat B(−/−) hepatocytes, as assessed by a fluorescence-based assay. With the use of a calcein release assay in isolated lysosomes, sphingosine permeabilized liver lysosomes isolated from Cat B(+/+) but not Cat B(−/−) liver. C6ceramide did not permeabilize lysosomes. In conclusion, these data implicate a sphingosine-Cat B interaction inducing lysosomal destabilization during TNF-α cytotoxic signaling.

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