scholarly journals Brassica juncea L. (Mustard) Extract Silver NanoParticles and Knocking off Oxidative Stress, ProInflammatory Cytokine and Reverse DNA Genotoxicity

Biomolecules ◽  
2020 ◽  
Vol 10 (12) ◽  
pp. 1650
Author(s):  
Sohair Aly Hassan ◽  
Ali Mohamed El Hagrassi ◽  
Olfat Hammam ◽  
Abdelmohsen M. Soliman ◽  
Essam Ezzeldin ◽  
...  
Keyword(s):  
Liver Failure ◽  
Proinflammatory Cytokine ◽  
Tumor Necrosis ◽  
Total Bilirubin ◽  
Ethanolic Extract ◽  
Ethanol Extract ◽  
Male Rats ◽  
Tnf Α ◽  
Liver Functions ◽  
Necrosis Factor

Detoxification is one of the main vital tasks performed by the liver. The purpose of this study was to investigate whether mustard in its normal or nanoparticles could confer a protective/therapeutic effect against TAA-induced acute liver failure in experimental animal models. Mustard ethanolic extract was analyzed by HPLC/MS. To induce liver failure, male rats were injected with 350 mg/kg bw TAA IP, then treated orally with a dose of 100 mg/kg for 15 d of mustard extract and its nanoform before and following induction. The levels of serum liver functions, total cholesterol (TCHo), total glyceride (TG), total bilirubin (TBIL), hepatic malonaldhyde (MDA) and nitric oxide (NO),glutathione (GSH), sodium oxide dismutase (SOD), as well as tumor necrosis factor (TNF-α,) and interleukin 6 (IL-6), were estimated. DNA genotoxicity and hepatic pathology, and immunohistologic (IHC) changes were assayed. The antioxidant content of Phenolic acids, flavonoids in mustard ethanolic extract substantially decreased the levels of ALT, AST, ALP and rehabilitated the histopathological alterations. In addition, nanoforms of mustard ethanol extract have notably increased the levels of GSH, SOD and significantly reduced the levels of MDA. The expression levels of TNF-α and IL-6 in serum and tissue were markedly downregulated. DNA genotoxicity was significantly reversed. Mustard introduced a protective and medicinal effect against TAA in both its forms.

Abstract P210: Central Blockade Of Tumor Necrosis Factor-Á-Converting Enzyme (tace) Ameliorates Neuroinflammation, Sympathetic Excitation And Cardiac Dysfunction In Heart Failure Rat

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Yang Yu ◽  
Baojian Xue ◽  
Hanzeng Li ◽  
Qing Chen ◽  
Mingxuan Li ◽  
...  
Keyword(s):  
Heart Failure ◽  
Body Weight ◽  
Growth Factor ◽  
Tumor Necrosis Factor ◽  
Cardiac Dysfunction ◽  
Tumor Necrosis ◽  
Left Ventricular ◽  
Male Rats ◽  
Tnf Α ◽  
Necrosis Factor

TACE is a key metalloprotease involved in ectodomain shedding of tumor necrosis factor (TNF)-α and transforming growth factor (TGF)-α. We previously reported that TACE-mediated production of TNF-α in the hypothalamic paraventricular nucleus (PVN) contributes to the sympathetic excitation in heart failure (HF). Additionally, the upregulated TGF-α in the PVN transactivates the epidermal growth factor receptor (EGFR) to activate extracellular signal-regulated kinase (ERK) 1/2 in HF. Here we sought to determine whether central inhibition of TACE attenuates neuroinflammation and prevents the progress of HF. Male rats underwent coronary artery ligation to induce HF or sham surgery (Sham). These rats were treated with bilateral PVN microinjection of a TACE siRNA or control siRNA while some rats received a 4-week intracerebroventricular (ICV) infusion of TACE inhibitor TAPI-0 or vehicle. Compared with Sham rats, HF rats treated with control siRNA, had higher (*P<0.05) levels of TNF-α (7.88±1.32* vs 2.77±0.98 pg/mL) and TGF-α (28.27±2.76* vs 11.62±2.48 pg/mL) in cerebrospinal fluid, and increased mRNA expression of TACE (2.53±0.30* vs 1.04±0.12), TNF-α (3.43±0.55* vs 1.03±0.11), TNF-α receptor 1 (2.32±0.27* vs 1.07±0.19), cyclooxygenase-2 (2.96±0.31* vs 1.10±0.19) and TGF-α (2.68±0.41* vs 1.06±0.14) in the PVN, but these levels were markedly reduced (39-54%*) in TACE siRNA-treated HF rats. Compared with control HF rats, HF rats treated with TACE siRNA had reduced expression of phosphorylated (p-) NF-κB p65 (1.27±0.14 vs 0.84±0.07*), p-EGFR (0.52±0.05 vs 0.37±0.04*) and p-ERK1/2 (1.06±0.10 vs 0.62±0.09*) in the PVN. Moreover, the elevated plasma norepinephrine levels, lung/body weight, heart/body weight and left ventricular (LV) end-diastolic pressure along with decreased LV dP/dt max in HF rats-treated with control siRNA were significantly attenuated in HF rats treated with TACE siRNA. Treatments with TACE siRNA in the PVN also improved the indicators of cardiac hypertrophy and fibrosis of HF. ICV infusion of TAPI-0 had the similar effects with PVN TACE siRNA on these variables in HF. These data indicate that central interventions suppressing TACE activity ameliorate neuroinflammation, sympathetic activation and cardiac dysfunction in HF.

Abstract P317: Sex Differences in the Hemodynamic and Sympathetic Responses to Centrally Administered Tumor Necrosis Factor-α in Rats

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Shun-Guang Wei ◽  
Yang Yu ◽  
Robert B Felder
Keyword(s):  
Heart Failure ◽  
Sex Differences ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Female Rats ◽  
Male Rats ◽  
Tnf Α ◽  
Estrogen Effect ◽  
Factor Α ◽  
Necrosis Factor

Introduction: Accumulating evidence indicates that sex differences exist in the clinical and experimental outcomes of various cardiovascular diseases. In addition to its protective effect on renin-angiotensin system activity, estrogen has an anti-inflammatory influence. The central actions of pro-inflammatory cytokines (PICs) contribute significantly to cardiovascular and autonomic dysfunction in hypertension and heart failure. In male adult rat, central administration of PICs induces substantial increases in blood pressure (BP), heart rate (HR) and renal sympathetic nerve activity (RSNA), and blocking PICs reduces sympathetic excitation in experimental models of hypertension and heart failure. Whether PICs have similar central sympatho-excitatory effects in the female rat remains unknown. Hypothesis: We hypothesized that female rats may be protected from the central cardiovascular and autonomic effects of PICs. Methods: Urethane anesthetized male and female Sprague Dawley rats (10-12 weeks) underwent an intracerebrovascular (ICV) injection of the prototypical PIC tumor necrosis factor-α (TNF-α, 100 ng). BP (mmHg), HR (beats/min) and RSNA (% change) responses were continuously recorded for 4-5 hours. Results: In male rats (n=6), ICV TNF-α induced a dramatic and long-lasting increase (*p<0.001 vs. baseline) in BP (23.1 ± 2.5*), HR (82 ± 8*) and RSNA (109.5 ± 4.3 %*), that began within 20-30 mins and peaked at 90-120 mins after ICV injection. In the female rats (n=6), ICV TNF-α elicited significantly (p<0.05) smaller increases (*p<0.001 vs. baseline) in BP (14.8 ± 1.8*), HR (55 ± 6*) and RSNA (78.5 ± 6.3*), compared with the male rats. Conclusion: These data demonstrate a sex difference in the cardiovascular and sympathetic responses to centrally administered PICs. Whether the observed differences can be explained by an estrogen effect on TNF-α signaling per se or by an estrogen effect on TNF-α-induced renin-angiotensin activity remains to be determined. However, a reduced response of female rats to central inflammation may be an important contributor to sex differences in pathophysiology of hypertension and heart failure.

A role for PKC-δ and PI 3-kinase in TNF-α-mediated antiapoptotic signaling in the human neutrophil

2002 ◽  
Vol 283 (1) ◽  
pp. C48-C57 ◽  
Author(s):  
Laurie E. Kilpatrick ◽  
Julia Y. Lee ◽  
Kathleen M. Haines ◽  
Donald E. Campbell ◽  
Kathleen E. Sullivan ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Protein Synthesis ◽  
Proinflammatory Cytokine ◽  
Tumor Necrosis ◽  
Spontaneous Apoptosis ◽  
Kinase C ◽  
Tnf Α ◽  
Cytokine Tumor Necrosis Factor ◽  
Transcription Factor Nfκb ◽  
Necrosis Factor

The proinflammatory cytokine tumor necrosis factor (TNF)-α has been implicated in the attenuation of neutrophil spontaneous apoptosis during sepsis. Antiapoptotic signaling is principally mediated through the p60TNF receptor (p60TNFR). In neutrophils, TNF-α is an incomplete secretagogue and requires input from a ligated integrin(s) for neutrophil activation. In adherent neutrophils, TNF-α triggers association of both protein kinase C (PKC)-δ and phosphatidylinositol (PI) 3-kinase with the p60TNFR. In this study, a role for PKC-δ and PI 3-kinase in TNF-α-mediated antiapoptotic signaling was examined. TNF-α inhibited spontaneous apoptosis in fibronectin-adherent neutrophils, and this antiapoptotic signaling was blocked by the PKC-δ inhibitor rottlerin, but not by an inhibitor of Ca2+-dependent PKC isotypes, Go-6976. Inhibition of PI 3-kinase by LY-294002 also inhibited TNF-α-mediated antiapoptotic signaling. Cycloheximide blocked TNF-α-mediated antiapoptotic signaling, suggesting protein synthesis is required. Inhibition of either PKC-δ or PI 3-kinase attenuated TNF-α-mediated activation of the antiapoptotic transcription factor NFκB. Thus both PKC-δ and PI 3-kinase have essential roles in TNF-α-mediated antiapoptotic signaling in adherent neutrophils.

scholarly journals Immunomodulatory Activity of Xestospongia sp. Ethanolic Extract Towards Interferon-gamma (IFN- γ) and Tumor Necrosis Factor-alpha (TNF-α) Levels in Wistar Male Rats

2020 ◽  
Vol 6 (2) ◽  
Author(s):  
Adryan Fristiohady ◽  
Jumadil ◽  
Wahyuni ◽  
Muh. Hajrul Malaka ◽  
Wa Ode Harnita ◽  
...  
Keyword(s):  
Ethanolic Extract ◽  
Group Iv ◽  
Male Rats ◽  
Immunomodulatory Activity ◽  
Necrosis Factor Alpha ◽  
Group Iii ◽  
Tnf Α ◽  
Factor Alpha ◽  
Ifn Γ ◽  
Necrosis Factor

Xestospongia sp. is one of marine sponge belongs to demosponges class that mainly found in Southeast Sulawesi and the secondary metabolites contained in Xestospongia sp. suspected to have immunomodulatory activity. A previous study exhibited the immunomodulatory of Xestospongia sp. ethanolic extract (XEE) at dose of 300 and 400 mg/Kg BW by affecting the phagocytic activity of macrophages. Thus, this study aims to investigate the effect of XEE towards interferon-gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α) at dose of 300 and 400 mg/Kg BW. Wistar male rats are divided into 4 groups (n=6) randomly and treated for 7 days orally each as follow: group I (XEE dose of 300 mg/KgBW); group II (XEE dose of 400 mg/KgBW); group III (0.5% NaCMC); and group IV (commercial phylantii extract). On day 8, animals were infected with Staphylococcus aureus and left for 1 hour. Animals were sacrificed and the blood was drawn by cardiac puncture (3 mL), followed by analyzed under ELISA Kit for IFN-γ and TNF-α. Collected data were analyzed statistically using SPSS®. The IFN-γ levels obtained were 350.113; 392.970; 118.416; and 61.958 ρg/mL, respectively and the TNF-α were 2808; 1308; 778; and 845.5 ρg/mL, respectively. According to results obtained, both doses of XEE are affecting the IFN-γ and TNF-α levels (p<0.05) compared to group III as negative control, and group IV as positive control. As conclusion, XEE of both doses is increasing IFN-γ and TNF-α levels of animals that respond to phagocytic activity

Comparisons of the Effects of Anesthesia and Stress on Release of Tumor Necrosis Factor-α, Leptin, and Nitric Oxide in Adult Male Rats

2001 ◽  
Vol 226 (4) ◽  
pp. 296-300 ◽  
Author(s):  
Claudio A. Mastronardi ◽  
Wen H. Yu ◽  
Samuel M. McCann
Keyword(s):  
Nitric Oxide ◽  
Tumor Necrosis Factor ◽  
Adult Male ◽  
Tumor Necrosis ◽  
Fold Increase ◽  
Male Rats ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Bacterial lipopolysaccharide (LPS) stimulates massive release of tumor necrosis factor-alpha (TNF-α) together with nitric oxide (NO) and a lessor release of leptin. We hypothesized that other types of stress such as that of surgery might also release these cytokines and NO. Adult male rats were anesthetized with ketamine/acepromazine/xylazine anesthesia (90 + 2 + 6 mg/ml, respectively) and an external jugular catheter was inserted for removal of blood samples (0.6 ml) at various times postoperatively. Plasma TNF-α was almost undetectable in decapitated rats and was near zero immediately following the placement of the jugular catheter (time zero [to]). As the rats awakened from anesthesia, there was a rise in TNF-α at 30 min that peaked at 2 hr with a 400-fold increase and then precipitously declined 40-fold to a level still greater than zero at 3 hr. At 6 hr on the following morning, TNF-α values were near zero, but following connection of tubing and withdrawal of the initial blood sample, there was a 100-fold increase 1 hr later, followed by a decline over the next 3 hr. In contrast, plasma [NO3/NO2] from decapitated rats was 117 μM. Values at t0 were decreased and plummeted 4-fold within 30 min, then rose slightly in the ensuing 3 hr. At 6 hr on the next day [NO3/NO2] values were lower than at t0 and declined gradually during the next 4 hr. Leptin gradually declined from pre-operative concentrations, reaching a minimum at 3 hr and its concentration was unaffected by the bleeding stress of the second day. We conclude that release of TNF-α, [NO3/NO2], and leptin are neurally controlled since plasma levels of all three declined as a result of anesthesia. TNF-α secretion was remarkably stress responsive, whereas NO release appeared to be suppressed by the combined operative and bleeding stress, and leptin was stress unresponsive.

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.

scholarly journals THE COMPARISON OF PROPOLIS EFFECTS ON TUMOR NECROSIS FACTOR ALPHA AND MALONDIALDEHYDE BETWEEN INHALATION AND CUTANEOUS ANTHRAX ANIMAL MODELS

2021 ◽  
Vol 16 (1) ◽  
pp. 1-5
Author(s):  
Dhani Redhono Harioputro ◽  
Wisnu Sanjaya ◽  
Yulyani Werdiningsih
Keyword(s):  
Animal Models ◽  
Tumor Necrosis ◽  
Ethanolic Extract ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Inhalation Anthrax ◽  
Cutaneous Anthrax ◽  
Factor Alpha ◽  
Ethanolic Extract Of Propolis ◽  
Necrosis Factor

Background: Inflammatory response and oxidative stress can be found in anthrax characterized by increased level of serum Tumor Necrosis Factor Alpha (TNF-α) and Malondialdehyde (MDA). The use of antibiotics in anthrax has been known to cause some disturbing side-effects, such as allergic reaction, nausea, vomiting, and antibiotic resistance. Thus, ethanolic extract of propolis (EEP) might be the alternative regimen, due to its anti-inflammatory and antioxidant properties. This study aimed to compare the effects of ethanolic extract of propolis (EEP) on TNF-α and MDA between the inhalation and cutaneous anthrax animal model. Materials and Methods: This was an experimental study with a post-test-only control group design on 40 samples of Rattus norvegicus. Samples were randomized into 5 groups: control, inhalation anthrax model, inhalation anthrax model + EEP, cutaneous anthrax model, and cutaneous anthrax model + EEP. After 14 days, the level of TNF-α and MDA were measured. To compare the data, we used the ANOVA test continued by the post-hoc Turkey test. Results: The results obtained showed that the level of TNF-α and MDA between the inhalation and cutaneous anthrax animal models treated with EEP were statistically different (p < 0.05). The P5 group showed the lowest level of TNF-α (6.822 ± 0.383 pg/ml) and MDA (2.717 ± 0.383 nmol/ml). Conclusion: EEP has a better effect on reducing TNF-α and MDA in cutaneous anthrax animal models compared to the inhalation anthrax animal model.

Effect of nutrition on tumor necrosis factor receptors in weight-gaining and -losing rats

1999 ◽  
Vol 277 (3) ◽  
pp. E464-E473 ◽  
Author(s):  
Nilima Raina ◽  
Jonathan Lamarre ◽  
Choong-Ching Liew ◽  
Amir H. Lofti ◽  
Khursheed N. Jeejeebhoy
Keyword(s):  
Plasma Membrane ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Energy Restriction ◽  
Male Rats ◽  
Northern Analysis ◽  
Cellular Expression ◽  
Protein Energy ◽  
Tnf Α ◽  
Necrosis Factor

Previous studies showed that weight-gaining rats had greater retention and reduced turnover of125I-labeled tumor necrosis factor (TNF)-α in the circulation compared with weight-losing animals. We therefore tested the hypothesis that protein-energy restriction with weight loss reduces the levels of soluble TNF-α receptor (sTNFR) and membrane TNFR (mTNFR) and the cellular expression of TNF-α mRNA. Twenty-six male rats weighing 200–220 g were fed a liquid formula diet for 10 days and divided equally into weight-gaining rats meeting all nutritional requirements (WG rats) and weight-losing rats with protein-energy restriction (WL rats).125I-TNF-α binding was demonstrated in plasma and plasma membrane to proteins of molecular masses of 92 and 243 kDa, a finding identical to that seen with purified human p55. Excess unlabeled TNF-α displaced the binding showing its specificity. The degree of binding to plasma protein and liver plasma membrane was markedly reduced in WL rats. Northern analysis showed that the expression of p55 mRNA was increased in the lungs and reduced in kidneys of WL compared with WG rats. The expression of p75 mRNA was not influenced by the nutritional status. We conclude that levels of sTNFR and mTNFR were reduced in WL rats. Reduced sTNFR and liver mTNFR are not due to a reduction in the expression of either p55 or p75 mRNA in WL rats. Reduced mTNFR, together with reduced shedding of soluble receptors, may have a protective role in WL rats.

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 Anti-Inflammatory Effects of Aurantiochytrium limacinum 4W-1b Ethanol Extract on Murine Macrophage RAW264 Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Shinya Takahashi ◽  
Masaki Yoshida ◽  
Makoto M. Watanabe ◽  
Hiroko Isoda
Keyword(s):  
Proinflammatory Cytokine ◽  
Tumor Necrosis ◽  
Inflammatory Responses ◽  
Ethanol Extract ◽  
No Production ◽  
Murine Macrophage ◽  
Macrophage Cells ◽  
Anti Inflammatory ◽  
Ethanol Extracts ◽  
Necrosis Factor

Aurantiochytrium limacinum 4W-1b (AL4W-1b) is a newly discovered microalgal strain with unique features. In the present study, we investigated the effects of ethanol extracts of AL4W-1b on lipopolysaccharide- (LPS-) induced inflammatory responses in RAW264 murine macrophage cells. Pretreatment of RAW264 cells with the AL4W-1b extract significantly reduced the production of LPS-induced nitric oxide (NO) and the expression of proinflammatory cytokine genes, including tumor necrosis factor α, interleukin- (IL-) 1β, and IL-6. Treatment with the AL4W-1b extract also decreased the production of IL-1β and IL-6. These results suggest that AL4W-1b might have anti-inflammatory effects in RAW264 cells. The NF-κB inhibitor, BAY 11-7082, synergistically prevented LPS-induced NO production after pretreatment with the AL4W-1b extract. Thus, the AL4W-1b extract may affect not only the NF-κB pathway but also other inflammatory pathways. To the best of our knowledge, this is the first study to report the anti-inflammatory effects of AL4W-1b extract and its mechanism of action in LPS-stimulated murine macrophage cells.

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