scholarly journals Effect of different anesthetic methods on cellular immune functioning and the prognosis of patients with ovarian cancer undergoing oophorectomy

2017 ◽  
Vol 37 (5) ◽  
Author(s):  
Xin-Rui Han ◽  
Xin Wen ◽  
Yan-Yi Li ◽  
Shao-Hua Fan ◽  
Zi-Feng Zhang ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Ovarian Cancer ◽  
Ca 125 ◽  
Red Cell ◽  
Post Surgery ◽  
Tnf Α ◽  
C3b Receptor ◽  
Factor Α ◽  
Cellular Immune ◽  
Necrosis Factor

The present study aimed to explore the effects of different anesthetic methods on cellular immune function and prognosis of patients with ovarian cancer (OC) undergoing oophorectomy. A total of 167 patients who received general anesthesia (GA) treatment (GA group) and 154 patients who received combined general/epidural anesthesia (GEA) treatment (GEA group) were collected retrospectively. Each group selected 124 patients that met the inclusion and exclusion criteria for further study. ELISA and radioimmunoassay were employed to detect levels of IL-2, TNF-α, and CA-125. The rates of tumor-red cell rosette (RTRR), red cell immune complex rosette (RRICR), and red cell C3b receptor rosette (RRCR) were also measured. Systolic blood pressure (SBP), diastolic blood pressure (DBP), and heart rate (HR) were determined by hemodynamics. The levels of tumor necrosis factor-α (TNF-α) and interleukin (IL)-2 decreased at 1 h intraoperation (T2), but increased 24-h post surgery (T3). The levels of TNF-α and IL-2 were recovered faster in the GEA group than in the GA group. The GA group exhibited greater levels of CA-125 expression than in the GEA group. The levels of RTRR, RRICR, and RRCR; ratios of CD3+, CD4+, CD4+/CD8+, CD16+, and CD56+ at 30 min after anesthesia (T1), T2, T3 and 48 h after the operation (T4) and levels of SBP, DBP, and HR at T1, T2, and T3 displayed increased levels in the GEA group than in the GA group. At 72-h post surgery (T5), the 5-year survival rate significantly increased in the GEA group compared with the GA group. GEA to be more suitable than GA for surgery on OC patients.

scholarly journals Tumor necrosis factor-α: regulation of renal function and blood pressure

2013 ◽  
Vol 304 (10) ◽  
pp. F1231-F1242 ◽  
Author(s):  
Vanesa D. Ramseyer ◽  
Jeffrey L. Garvin
Keyword(s):  
Blood Pressure ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Immune Cell ◽  
Organ Damage ◽  
Physiological Status ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Tumor necrosis factor-α (TNF-α) is a pleiotropic cytokine that becomes elevated in chronic inflammatory states such as hypertension and diabetes and has been found to mediate both increases and decreases in blood pressure. High levels of TNF-α decrease blood pressure, whereas moderate increases in TNF-α have been associated with increased NaCl retention and hypertension. The explanation for these disparate effects is not clear but could simply be due to different concentrations of TNF-α within the kidney, the physiological status of the subject, or the type of stimulus initiating the inflammatory response. TNF-α alters renal hemodynamics and nephron transport, affecting both activity and expression of transporters. It also mediates organ damage by stimulating immune cell infiltration and cell death. Here we will summarize the available findings and attempt to provide plausible explanations for such discrepancies.

scholarly journals Angiotensin receptor and tumor necrosis factor-α activation contributes to glucose intolerance independent of systolic blood pressure in obese rats

2018 ◽  
Vol 315 (4) ◽  
pp. F1081-F1090 ◽  
Author(s):  
Ruben Rodriguez ◽  
Andrew Lee ◽  
Keisa W. Mathis ◽  
Hanna J. Broome ◽  
Max Thorwald ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Glucose Intolerance ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Angiotensin Receptor Blocker ◽  
Angiotensin Receptor ◽  
Tnf Α ◽  
Long Evans ◽  
Factor Α ◽  
Necrosis Factor

Pathological activation of the renin-angiotensin system and inflammation are associated with hypertension and the development of metabolic syndrome (MetS). The contributions of angiotensin receptor type 1 (AT1) activation, independent of blood pressure, and inflammation to glucose intolerance and renal damage are not well defined. Using a rat model of MetS, we hypothesized that the onset of glucose intolerance is primarily mediated by AT1 activation and inflammation independent of elevated systolic blood pressure (SBP). To address this hypothesis, we measured changes in SBP, adiposity, plasma glucose and triglyceride levels, and glucose tolerance in six groups of rats: 1) lean, strain control Long-Evans Tokushima Otsuka (LETO; n = 5), 2) obese Otsuka Long-Evans Tokushima Fatty (OLETF; n = 8), 3) OLETF + angiotensin receptor blocker (ARB; 10 mg olmesartan/kg; n = 8), 4) OLETF + tumor necrosis factor-α (TNF-α) inhibitor (ETAN; 1.25 mg etanercept/kg; n = 6), 5) OLETF + TNF-α inhibitor + angiotensin receptor blocker (ETAN+ARB; 1.25 mg etanercept/kg + 10 mg olmesartan/kg; n = 6), and 6) OLETF + calcium channel blocker (CCB; 5 mg amlodipine/kg; n = 7). ARB and ETAN+ARB were most effective at decreasing SBP in OLETF, and ETAN did not offer any additional reduction. Glucose tolerance improved in ARB, ETAN, and ETAN+ARB compared with OLETF, whereas CCB had no detectable effect. Furthermore, all treatments reduced adiposity, whereas ETAN alone normalized urinary albumin excretion. These results suggest that AT1 activation and inflammation are primary factors in the development of glucose intolerance in a setting of MetS and that the associated increase in SBP is primarily mediated by AT1 activation.

scholarly journals Oxidative stress and biomarker of TNF-α, MDA and FRAP in hypertension

2019 ◽  
Vol 12 (3) ◽  
pp. 253-259 ◽  
Author(s):  
Manish Kumar Verma ◽  
◽  
Anoop Jaiswal ◽  
Preeti Sharma ◽  
Pradeep Kumar ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Tumor Necrosis Factor ◽  
High Blood Pressure ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Hypertensive Patients ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Concurrent with the misbalance of oxidizing agents and antioxidants, high blood pressure is a major physical burden condition in the current scenario. Tumor necrosis factor-α (TNF-α) plays a vital role in the pathogenesis of hypertension. Tumor necrosis factor-α, inhibitor improves clinical symptoms however their outcome on high blood pressure has not been investigated. We investigated the inflammatory marker TNF-α, malondialdehyde (MDA) and ferric reducing antioxidant power (FRAP) in hypertensive patients. We measured randomly blood pressure using an ambulatory observe in hypertensive patients, measured systolic BP X 140 mmHg and/or diastolic BP X 90 mmHg were considered hypertensive. Total 60 cases were considered in the study that involves 30 hypertensive patients and 30 normal control. Measurements of serum concentrations of TNF-α, MDA, FRAP in hypertension patients was done in both the groups. Serum TNF-α was found to be remarkably increased in study subjects as compared to normal group (r=0.32, p<0.0001*). Serum MDA was also raised in hypertensive as compared to control (r=0.99**, p<0.0001*). While Serum FRAP was found to be decreased in hypertensive group in comparison to healthy control (r=0.23, p<0.0001*). It is concluded that high blood pressure leads to generation of oxidative stress with remarkable elevation of TNF-α and malondialdehyde levels. While reduced FRAP indicates its probable role in lipid peroxidation and in the pathogenesis of hypertension.

scholarly journals Anti-Inflammatory Effect of Simonsinol on Lipopolysaccharide Stimulated RAW264.7 Cells through Inactivation of NF-κB Signaling Pathway

Molecules ◽  
2020 ◽  
Vol 25 (16) ◽  
pp. 3573
Author(s):  
Lian-Chun Li ◽  
Zheng-Hong Pan ◽  
De-Sheng Ning ◽  
Yu-Xia Fu
Keyword(s):  
Nitric Oxide ◽  
Signaling Pathway ◽  
Morphological Changes ◽  
Raw264.7 Cells ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Oxide Synthase ◽  
Necrosis Factor

Simonsinol is a natural sesqui-neolignan firstly isolated from the bark of Illicium simonsii. In this study, the anti-inflammatory activity of simonsinol was investigated with a lipopolysaccharide (LPS)-stimulated murine macrophages RAW264.7 cells model. The results demonstrated that simonsinol could antagonize the effect of LPS on morphological changes of RAW264.7 cells, and decrease the production of nitric oxide (NO), tumor necrosis factor α (TNF-α), and interleukin 6 (IL-6) in LPS-stimulated RAW264.7 cells, as determined by Griess assay and enzyme-linked immunosorbent assay (ELISA). Furthermore, simonsinol could downregulate transcription of inducible nitric oxide synthase (iNOS), TNF-α, and IL-6 as measured by reverse transcription polymerase chain reaction (RT-PCR), and inhibit phosphorylation of the alpha inhibitor of NF-κB (IκBα) as assayed by Western blot. In conclusion, these data demonstrate that simonsinol could inhibit inflammation response in LPS-stimulated RAW264.7 cells through the inactivation of the nuclear transcription factor kappa-B (NF-κB) signaling pathway.

#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

Tumor Necrosis Factor-α Production-Enhancing Properties of Novel Adamantylalkylthio Derivatives of Some Heterocyclic Compounds

2005 ◽  
Vol 60 (4) ◽  
pp. 471-475 ◽  
Author(s):  
Barbara Orzeszko ◽  
Tomasz Świtaj ◽  
Anna B. Jakubowska-Mućka ◽  
Witold Lasek ◽  
Andrzej Orzeszko ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Heterocyclic Compounds ◽  
Tumor Necrosis ◽  
The Novel ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Factor Α ◽  
Derivatives Of ◽  
Necrosis Factor

Certain adamantylated heterocycles were previously shown to enhance the secretion of tumor necrosis factor alpha (TNF-α) by murine melanoma cells that have been transduced with the gene for human TNF-α and constitutively expressed this cytokine. The stimulatory potency of those compounds depended, among other factors, on the structure of the linker between the adamantyl residue and the heterocyclic core. In the present study, a series of (1-adamantyl)alkylsulfanyl derivatives of heterocyclic compounds was prepared by alkylation of the corresponding thioheterocyles. Of the novel adamantylalkylthio compounds tested in the aforementioned cell line, 2-(2-adamantan-1-ylethylsulfanyl)- 4-methyl-pyrimidine was found to be the most active

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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