scholarly journals Effect of Diosmin Administration in Patients with Chronic Venous Disorders on Selected Factors Affecting Angiogenesis

Molecules ◽  
2019 ◽  
Vol 24 (18) ◽  
pp. 3316 ◽  
Author(s):  
Marcin Feldo ◽  
Magdalena Wójciak-Kosior ◽  
Ireneusz Sowa ◽  
Janusz Kocki ◽  
Jacek Bogucki ◽  
...  
Keyword(s):  
Growth Factor ◽  
Clinical Symptoms ◽  
Lymphatic Drainage ◽  
Tnf Alpha ◽  
Ultrasound Images ◽  
Necrosis Factor Alpha ◽  
Factors Affecting ◽  
Wide Range ◽  
Before And After ◽  
Venous Disorders

Diosmin is a natural compound with a wide range of biological activity, e.g., it improves lymphatic drainage, supports microcirculation, and increases venous tone, and venous elasticity, hence, it is applied in the pharmacotherapy of chronic venous disorders (CVD). The aim of this study was to assess the correlation between diosmin administration (2 × 600 mg daily) in patients suffering from CVD and the levels of selected factors influencing angiogenesis, which are involved in CVD pathophysiology. Thirty-five CVD patients were examined. Levels of plasma tumor necrosis factor alpha (TNF alpha), vascular endothelial growth factor (VEGF-A and VEGF-C); angiostatin, interleukin 6 (IL-6), fibroblast growth factor 2 (FGF2); and plasminogen (PLG) were measured with an Elisa assay before and after three months of diosmin administration. The clinical symptoms of CVD were monitored using ultrasound images, echo Doppler assay, visual analogue scale (VAS), and measurement of the leg circumference. The average content of TNF alpha, VEGF-C, VEGF-A IL-6, and FGF2 decreased after the therapy with diosmin in a significant manner; with p < 0.001, p < 0.05, p < 0.05, p < 0.01, and p < 0.01, respectively, and a significant (p < 0.05) increase in the plasma angiostatin level after the three-month treatment was found. A significant (p < 0.05) decrease in edema and the average leg circumference of the patients was observed after the therapy. Diosmin influences the angiogenic and inflammatory mechanisms involved in the pathophysiology of edema presented in patients with a different class of CVD.

scholarly journals Liver Growth Factor Induces Glia-Associated Neuroprotection in an In Vitro Model of Parkinson´s Disease

2020 ◽  
Vol 10 (5) ◽  
pp. 315
Author(s):  
Rafael Gonzalo-Gobernado ◽  
Diana Reimers ◽  
María José Casarejos ◽  
Lucía Calatrava Ferreras ◽  
Manuela Vallejo-Muñoz ◽  
...  
Keyword(s):  
Growth Factor ◽  
Neurodegenerative Disorder ◽  
Neuronal Degeneration ◽  
Neuroprotective Effect ◽  
Tnf Alpha ◽  
Sprague Dawley ◽  
Necrosis Factor Alpha ◽  
Liver Growth ◽  
Glial Cultures

Parkinson’s disease is a neurodegenerative disorder characterized by the progressive death of dopaminergic (DA) neurons in the substantia nigra (SN), which leads to a loss of the neurotransmitter dopamine in the basal ganglia. Current treatments relieve the symptoms of the disease, but none stop or delay neuronal degeneration. Liver growth factor (LGF) is an albumin–bilirubin complex that stimulates axonal growth in the striatum and protects DA neurons in the SN of 6-hydroxydopamine-lesioned rats. Our previous results suggested that these effects observed in vivo are mediated by microglia and/or astrocytes. To determine if these cells are LGF targets, E14 (embryos from Sprague Dawley rats of 14 days) rat mesencephalic glial cultures were used. Treatment with 100 pg/mL of LGF up-regulated the mitogen-activated protein kinases (MAPKs) extracellular signal-regulated kinases 1/2 (ERK1/2) and the cyclic AMP response element binding protein (CREB) phosphorylation in glial cultures, and it increased the microglia marker Iba1 and tumor necrosis factor alpha (TNF-alpha) protein levels. The treatment of E14 midbrain neurons with a glial-conditioned medium from LGF-treated glial cultures (GCM-LGF) prevented the loss of DA neurons caused by 6-hydroxy-dopamine. This neuroprotective effect was not observed when GCM-LGF was applied in the presence of a blocking antibody of TNF-alpha activity. Altogether, our findings strongly suggest the involvement of microglia and TNF-alpha in the neuroprotective action of LGF on DA neurons observed in vitro.

scholarly journals Interleukin-4 inhibits both paracrine and autocrine tumor necrosis factor-alpha-induced proliferation of B chronic lymphocytic leukemia cells

Blood ◽  
1992 ◽  
Vol 80 (5) ◽  
pp. 1299-1306 ◽  
Author(s):  
C van Kooten ◽  
I Rensink ◽  
L Aarden ◽  
R van Oers
Keyword(s):  
Growth Factor ◽  
Chronic Lymphocytic Leukemia ◽  
Tumor Necrosis Factor ◽  
Proliferative Response ◽  
Tumor Necrosis ◽  
Lymphocytic Leukemia ◽  
Interleukin 4 ◽  
Tnf Alpha ◽  
Necrosis Factor Alpha ◽  
Necrosis Factor

Abstract The proliferative response of purified malignant B cells from 26 patients with chronic lymphocytic leukemia (CLL) was investigated in vitro. In the majority of these patients, a proliferative response could be induced by the combination of tumor necrosis factor (TNF)- alpha and PMA. The concentration of PMA was found to be critical and showed a sharp optimum. In most cases maximal proliferation was obtained with as little as 0.1 ng/mL PMA. In all cases tested, TNF- alpha-induced proliferation could be inhibited completely by the addition of low doses of interleukin-4 (IL-4). Maximal inhibition was already found with 400 pg/mL IL-4. Inhibition by IL-4 was not caused by a downmodulation of TNF receptors. Apart from TNF-alpha, IL-2 was also in synergy with PMA able to induce proliferation in B-CLL cells of some patients. This IL-2-induced proliferation could be inhibited both by IL- 4 and by neutralizing anti-TNF-alpha antibodies. This shows that TNF- alpha also can act as an autocrine growth factor. These data indicate that TNF-alpha is an important growth factor for neoplastic B-CLL cells and that IL-4 provides a tool to interfere with this TNF-alpha response.

scholarly journals Prognostic Factors of Grade 2-3 Endo-Periodontal Lesions Treated Nonsurgically in Patients with Periodontitis: A Retrospective Case-Control Study

2020 ◽  
Vol 2020 ◽  
pp. 1-9 ◽  
Author(s):  
Xiaomiao Fan ◽  
Xiaoyu Xu ◽  
Shiwen Yu ◽  
Peicheng Liu ◽  
Chen Chen ◽  
...  
Keyword(s):  
Logistic Regression ◽  
Clinical Symptoms ◽  
Univariate Analysis ◽  
Clinical Parameters ◽  
Retrospective Case ◽  
Factors Affecting ◽  
Root Canals ◽  
Before And After ◽  
Low Responder ◽  
Poor Outcomes

Background. Endo-periodontal lesions are bacterial infectious diseases involving both the periodontal and pulp tissues with poor outcomes. It is hard for clinicians to predict their prognosis. The aim of this study is to investigate the factors affecting the prognosis of endo-periodontal lesions. Methods. A total of 140 teeth diagnosed with grade 2-3 endo-periodontal lesions in patients with periodontitis were recruited in this study. They were divided into high and low responder groups, according to the clinical symptoms and parameters of the teeth involved after nonsurgical treatment of both the endodontic and periodontal components. Clinical parameters and symptoms were compared before and after treatment, and gender, age, smoking, and all clinical parameters were compared between high and low responder groups using univariate analyses. Logistic regression was applied to evaluate the independent effects on endo-periodontal lesion prognosis. Results. Compared with the clinical parameters at baseline, the values of tooth mobility (TM), periapical index (PAI), and discomfort when chewing were decreased after endodontic therapy, and the values of periodontal probing depth (PD), clinical attachment level (CAL), sulcus bleeding index (SBI), TM, simplified oral hygiene index (OHI-S), full-mouth periodontitis severity, PAI, and discomfort when chewing were decreased after periodontal therapy. Univariate analysis revealed that smoking, PD, CAL, TM, PAI, clinical crown-root ratio (CR), full-mouth periodontitis severities, and the number of root canals were significantly different between the high and low responder groups (P<0.05). The logistic regression analysis showed that smoking, PD, CAL, full-mouth periodontitis severities, and the number of root canals remained significantly associated with grade 2-3 endo-periodontal lesions in patients with periodontitis (P<0.05). Conclusionsand Practical Implications. High PD and CAL, multirooted teeth, smoking, and serious full-mouth periodontitis indicated a poor prognosis for teeth with grade 2-3 endo-periodontal lesions.

scholarly journals Interleukin-4 inhibits both paracrine and autocrine tumor necrosis factor-alpha-induced proliferation of B chronic lymphocytic leukemia cells

Blood ◽  
1992 ◽  
Vol 80 (5) ◽  
pp. 1299-1306
Author(s):  
C van Kooten ◽  
I Rensink ◽  
L Aarden ◽  
R van Oers
Keyword(s):  
Growth Factor ◽  
Chronic Lymphocytic Leukemia ◽  
Tumor Necrosis Factor ◽  
Proliferative Response ◽  
Tumor Necrosis ◽  
Lymphocytic Leukemia ◽  
Interleukin 4 ◽  
Tnf Alpha ◽  
Necrosis Factor Alpha ◽  
Necrosis Factor

The proliferative response of purified malignant B cells from 26 patients with chronic lymphocytic leukemia (CLL) was investigated in vitro. In the majority of these patients, a proliferative response could be induced by the combination of tumor necrosis factor (TNF)- alpha and PMA. The concentration of PMA was found to be critical and showed a sharp optimum. In most cases maximal proliferation was obtained with as little as 0.1 ng/mL PMA. In all cases tested, TNF- alpha-induced proliferation could be inhibited completely by the addition of low doses of interleukin-4 (IL-4). Maximal inhibition was already found with 400 pg/mL IL-4. Inhibition by IL-4 was not caused by a downmodulation of TNF receptors. Apart from TNF-alpha, IL-2 was also in synergy with PMA able to induce proliferation in B-CLL cells of some patients. This IL-2-induced proliferation could be inhibited both by IL- 4 and by neutralizing anti-TNF-alpha antibodies. This shows that TNF- alpha also can act as an autocrine growth factor. These data indicate that TNF-alpha is an important growth factor for neoplastic B-CLL cells and that IL-4 provides a tool to interfere with this TNF-alpha response.

scholarly journals Overview of The Current Progress of Facultative Anaerobic Bacteria in Cancer Biotherapy with TNF-α as Main Mechanism of Action

2021 ◽  
Author(s):  
Martina Johansson ◽  
Fredrik Nystrom
Keyword(s):  
Side Effects ◽  
Cancer Treatment ◽  
Anaerobic Bacteria ◽  
Tnf Alpha ◽  
Biological Therapies ◽  
Necrosis Factor Alpha ◽  
Signalling Molecules ◽  
Genetically Engineer ◽  
Wide Range ◽  
Facultative Anaerobic Bacteria

This review article focuses on the use of infectious bacteria as delivery tool for tumour necrosis factor alpha, a well-studied cytokine, in the context of immunotherapy for cancer treatment. The tumour targeting properties of certain bacteria strains has been known for decades as well as the tumour catabolizing effect of TNF-alpha. The combination of these two have been studied in murine models for various types of cancer with promising results. Research in this fascinating field is unfortunately uncommon, thus the number of high-quality articles is limited. Search was done via Google Scholar in combination with PubMed, to increase the coverage and find peer-reviewed, original, and primary research articles. Key findings show that attenuated or genetically modified species of bacteria have fewer side effects and can be effective in delivering cytokines to tumour sites. TNF-alpha is produced by macrophages/monocytes during acute inflammation or infection, thus can be triggered by infectious bacteria which in turn induce apoptosis. The cytotoxic effect of the bacteria can be enhanced with localized irradiation. Promising results have been shown in bladder, breast, colon, glial, lung, ovarian, pancreatic, prostate, and renal cancer cells. The need for better, safer, and more effective cancer treatment is apparent as traditional chemotherapy and radiation can cause a lot of harm for the patient, and not necessarily prolong the lifespan. The success-rate for these treatments vary greatly depending on the type of cancer, but for tumours that cannot be surgically removed the outcome is generally quite poor. A drawback of chemotherapy is that tumours can grow resistant to the treatment while healthy cells continue to be exposed, increasing the risk of severe side effects. Different types of biological therapies are a modern and possibly safer approach, even though immunotherapy comes with substantial risks. Using the innate immune system to fight tumour cells is not always safe, because uncontrolled and excessive release of pro-inflammatory signalling molecules can result in multisystem organ failure and death. This phenomenon is called cytokine release syndrome (cytokine storm) and is one of the major risks of immunotherapy. However, tailored biological therapies have proven their effectiveness for a wide range of cancer types, and the next step in this evolution is to genetically engineer both delivery systems and mechanisms of action. This approach can be combined with the traditional radiation and chemotherapy for increased effectiveness, even if biological therapies as a stand-alone treatment, can be a goal for the future.

Modification of vascular reactivity by alteration of intimal permeability: effect of TNF-alpha

1993 ◽  
Vol 264 (6) ◽  
pp. H1847-H1853 ◽  
Author(s):  
T. Matsuki ◽  
J. M. Beach ◽  
R. L. Klindt ◽  
B. R. Duling
Keyword(s):  
Vascular Reactivity ◽  
Water Soluble ◽  
Tnf Alpha ◽  
Necrosis Factor Alpha ◽  
Small Water ◽  
Vasoactive Substances ◽  
Before And After ◽  
Arteriolar Wall ◽  
Factor Alpha ◽  
Cheek Pouches

We investigated the effects of alterations in intimal permeability on microvascular reactivity to small hydrophilic agents in isolated, cannulated, perfused arterioles (65 +/- 6 microns ID) from hamster cheek pouches. Arterioles are 300-fold less responsive to the hydrophilic alpha 1-agonist, phenylephrine, applied to the lumen than when applied to the adventitia. Luminal treatment with tumor necrosis factor-alpha (TNF-alpha, 0.625 micrograms/ml, 1–2 h) potentiated reactivity to luminally applied phenylephrine, but the treatment did not change reactivity to adventitially applied phenylephrine. Similar results were obtained with a brief treatment with the detergent, 3-[(3-cholamidopropyl)dimethylammonio]-1- propanesulfonate (CHAPS; 0.3%, < 30 s). To confirm that a change in permeability had occurred, we measured the movement across the arteriolar wall of a low-molecular-weight hydrophilic fluorescent molecule, fluorescein, before and after luminal treatment with TNF-alpha or CHAPS. Either TNF-alpha or CHAPS significantly increased the rate of movement of fluorescein across the arteriolar wall. These data suggest that one element in the pathophysiology of TNF-alpha is an increase in arteriolar permeability to small, water-soluble agents, which may modify reactivity to circulating vasoactive substances.

Correlation between GH and IGF-1 during treatment for acromegaly

2016 ◽  
Vol 126 (6) ◽  
pp. 1959-1966 ◽  
Author(s):  
Edward H. Oldfield ◽  
John A. Jane ◽  
Michael O. Thorner ◽  
Carrie L. Pledger ◽  
Jason P. Sheehan ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Response To Treatment ◽  
Gh Secretion ◽  
Wide Range ◽  
Before And After ◽  
Z Scores ◽  
Tumor Viability ◽  
The Relationship ◽  
Over Time

OBJECTIVEThe relationship between growth hormone (GH) and insulin-like growth factor–1 (IGF-1) in patients with acromegaly as serial levels drop over time after treatment has not been examined previously. Knowledge of this relationship is important to correlate pretreatment levels that best predict response to treatment. To examine the correlation between GH and IGF-1 and IGF-1 z-scores over a wide range of GH levels, the authors examined serial GH and IGF-1 levels at intervals before and after surgery and radiosurgery for acromegaly.METHODSThis retrospective analysis correlates 414 pairs of GH and IGF-1 values in 93 patients with acromegaly.RESULTSAbsolute IGF-1 levels increase linearly with GH levels only up to a GH of 4 ng/ml, and with IGF-1 z-scores only to a GH level of 1 ng/ml. Between GH levels of 1 and 10 ng/ml, increases in IGF-1 z-scores relative to changes in GH diminish and then plateau at GH concentrations of about 10 ng/ml. From patient to patient there is a wide range of threshold GH levels beyond which IGF-1 increases are no longer linear, GH levels at which the IGF-1 response plateaus, IGF-1 levels at similar GH values after the IGF-1 response plateaus, and of IGF-1 levels at similar GH levels.CONCLUSIONSIn acromegaly, although IGF-1 levels represent a combination of the integrated effects of GH secretion and GH action, the tumor produces GH, not IGF-1. Nonlinearity between GH and IGF-1 occurs at GH levels far below those previously recognized. To monitor tumor activity and tumor viability requires measurement of GH levels.

scholarly journals Involvement of interleukin-8, vascular endothelial growth factor, and basic fibroblast growth factor in tumor necrosis factor alpha-dependent angiogenesis.

1997 ◽  
Vol 17 (7) ◽  
pp. 4015-4023 ◽  
Author(s):  
S Yoshida ◽  
M Ono ◽  
T Shono ◽  
H Izumi ◽  
T Ishibashi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Vascular Endothelial Cells ◽  
Tnf Alpha ◽  
Vascular Endothelial ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Nf Kappab ◽  
Endothelial Growth Factor

Tumor necrosis factor alpha (TNF-alpha) is a macrophage/monocyte-derived polypeptide which modulates the expression of various genes in vascular endothelial cells and induces angiogenesis. However, the underlying mechanism by which TNF-alpha mediates angiogenesis is not completely understood. In this study, we assessed whether TNF-alpha-induced angiogenesis is mediated through TNF-alpha itself or indirectly through other TNF-alpha-induced angiogenesis-promoting factors. Cellular mRNA levels of interleukin-8 (IL-8), vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and their receptors were increased after the treatment of human microvascular endothelial cells with TNF-alpha (100 U/ml). TNF-alpha-dependent tubular morphogenesis in vascular endothelial cells was inhibited by the administration of anti-IL-8, anti-VEGF, and anti-bFGF antibodies, and coadministration of all three antibodies almost completely abrogated tubular formation. Moreover, treatment with Sp1, NF-kappaB, and c-Jun antisense oligonucleotides inhibited TNF-alpha-dependent tubular morphogenesis by microvascular endothelial cells. Administration of a NF-kappaB antisense oligonucleotide almost completely inhibited TNF-alpha-dependent IL-8 production and partially abrogated TNF-alpha-dependent VEGF production, and an Sp1 antisense sequence partially inhibited TNF-alpha-dependent production of VEGF. A c-Jun antisense oligonucleotide significantly inhibited TNF-alpha-dependent bFGF production but did not affect the production of IL-8 and VEGF. Administration of an anti-IL-8 or anti-VEGF antibody also blocked TNF-alpha-induced neovascularization in the rabbit cornea in vivo. Thus, angiogenesis by TNF-alpha appears to be modulated through various angiogenic factors, both in vitro and in vivo, and this pathway is controlled through paracrine and/or autocrine mechanisms.

scholarly journals Possible Alterations in the Plasma Levels of Pro (TNF-alpha) and Anti-inflammatory (IL-10) Cytokines in Long-Term Insomnia

2019 ◽  
Vol 5 ◽  
pp. 1
Author(s):  
Mathew F. Olaniyan ◽  
Alade Ogunlade ◽  
◽  
Keyword(s):  
Chronic Insomnia ◽  
Tnf Alpha ◽  
Infectious Agents ◽  
Necrosis Factor Alpha ◽  
Significant Difference ◽  
Before And After ◽  
Factor Alpha ◽  
Microbial Agents

Long-term/chronic insomnia occurs in patients for over one month; it can affect the functions of the immune system and responses, which may involve cytokines. The aim was to determine alterations of Tumor necrosis factor alpha (TNF-alpha) and IL-10 cytokines in long-term insomnia. Thirty-three long-term/chronic insomnia patients (male, 22; female, 11) aged 47-61 years were initially recruited. Seven of them who were infected with microbial agents were excluded from the study. Of the 26 free of infectious agents only 21 (female, 5; male, 16) were successfully monitored. Age-matched apparently healthy non-insomnia subjects (male, 25; female, 25) free of the infectious agents were recruited as control. Plasma TNF-alpha, IL-10, HBsAg, anti-HCV, and HIVp24 antigen were assayed by ELISA method while determination of Mycobacterium tuberculosis was by Ziehl–Neelsen staining of sputum and Plasmodium spp. by thick blood Giemsa staining. Of the 33 insomnia patients initially recruited, 21.2% (7) were infected with microbial agents (Plasmodium spp., 6.1% (2); HCV, 3.0% (1); HBV, 6.1% (2); Mycobacterium tuberculosis, 3.0% (1); Plasmodium spp. + HBV, 3.0% (1); and HIVp24, 0). Twenty-one chronic insomnia patients were finally investigated on cytokines. There were significantly higher mean plasma values of TNF-alpha and IL-10 cytokines in chronic insomnia patients before treatment than the values obtained in the control subjects (p < 0.05). The results also showed a significantly lower mean plasma value of TNF-alpha cytokine in chronic insomnia patients after treatment than the values obtained in the patients before treatment. There were no significant differences in the mean plasma values of IL-10 cytokines in chronic insomnia patients before and after treatment (p > 0.05). There was a significant increase in plasma TNF-alpha and IL-10 cytokines in long-term insomnia patients before treatment while plasma TNF-alpha significantly decreased after treatment, and no significant difference was obtained in the plasma IL-10 before and after treatment. TNF-alpha could be a good investigative index of insomnia.

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