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The association between norepinephrine and metabolism in patients with major depression

Posted by J Futtrup, M Nordentoft, B Elfving, et al. on 2018-07-19 18:51:09

Abstract

Background

Previous studies indicate that levels of plasma norepinephrine (p-NE) are altered in depressed patients. However, it is unclear whether altered NE metabolism is involved in the pathogenic association between depression and cardiovascular disease. The aim of the present study was, firstly, to investigate if p-NE levels differ between patients with major depression and healthy controls. Secondly, the study sought to assess the associations between p-NE and metabolic variables in all participants. The third and final aim of the study was to assess if the associations between p-NE and metabolic variables are influenced by disease status (depression vs. healthy).

Methods

108 patients with major depression and 44 healthy controls were tested for levels of p-NE and metabolic variables that affect cardiovascular risk.

Results

The median level of p-NE in depressed patients (DSM-IV) was 2636 pg/ml, (IQR 2094–3143) and 2279 pg/ml (IQR 2007–2562) in non-depressed controls (p = 0.013). However, the difference between p-NE levels was non-significant when adjusted for daily smoking (p = 0.138). Significant associations (p ≤ 0.05) were observed between p-NE and p-lipids, mean arterial blood pressure, p-insulin, quantitative insulin sensitivity check index as well as inflammatory markers.

Conclusions

Elevated levels of p-NE observed in patients with major depression were attributable to daily smoking, rather than to the depressive disorder. Important associations were found between p-NE and metabolic variables that affect cardiovascular risk. This is interesting from a clinical point of view, since affected individuals may benefit from simple and inexpensive treatments that influence sympathetic activity. All associations were independent of disease status.

Abstract

Background aims

TNFR family member glucocorticoid-induced tumor necrosis factor–related receptor (GITR/TNFRSF18) activation by its ligand glucocorticoid-induced TNF-related receptor ligand (GITRL) have important roles in proliferation, death and differentiation of cells. Some types of small cell lung cancers (SCLCs) express GITR. Because mesenchymal stromal cells (MSCs) may target tumor cells, we aimed to investigate the effect of MSCs carrying GITRL overexpressing plasmid on the proliferation and viability of a GITR+ SCLC cell line (SCLC-21H) compared with a GITR– SCLC cell line (NCI-H82).

Methods

Electroporation was used to transfer pGITRL (GITRL gene carrying plasmid) or pCR3 (mock plasmid) into MSCs. Flow cytometry and semi-quantitative polymerase chain reaction were used to characterize the transfected MSCs. Following SCLC-21H or NCI-H82 cell lines were co-cultured with pGITRL-MSCs.

Results

Proliferation of NCI-H82 was increased in all types of co-cultures while SCLC-21H cells did not. GITRL expressing MSCs were able to induce cell death of SCLC-21H through the upregulation of SIVA1 apoptosis inducing factor.

Conclusions

The influence of MSCs on SCLC cells can vary according to the cancer cell subtypes as obtained in SCLC-21H and NCI-H82 and enabling GITR-GITRL interaction can induce cell death of SCLC cell lines.

Key Words

apoptosis; cell-based gene delivery; genetically modified MSCs; GITRL; mesenchymal stromal cell; small cell lung cancer; SIVA

Abstract

Objectives

Angiogenesis underlies tumour growth and metastasis through hepatocyte growth factor (HGF), epithelial growth factor (EGF), and vascular endothelial growth factor (VEGF). The aim of this study was to determine the levels of VEGF, EGF, HGF, HGFR (hepatocyte growth factor receptor), and SRSF1 (serine-rich protein splicing factor-1) in patients with parotid gland tumours and in healthy controls via ELISA in parotid saliva. Immunohistochemical expression of anti-angiogenic isoform of VEGF165b subunit, VEGFR1, VEGFR2, and microvessel density (CD34) were assessed in the tumour tissue and in the non-tumorous surrounding margins.

Materials and methods

The study included 48 patients with benign and malignant parotid gland tumours and 15 healthy controls.

Results

Comparison of VEGF, EGF, and HGF in tumour and non-tumorous tissues showed no significant differences and no correlations with tumour stage. The salivary VEGF concentration was significantly higher in patients with pleomorphic adenoma and Warthin’s tumour. No significant correlation was found between expression of VEGF165b and VEGFR2 in tumours and non-tumor surgical margins.

Conclusions

The increased salivary VEGF reflects changes in affected parotid glands, but it cannot be used as a prognostic and differentiative factor for parotid tumours.

Clinical relevance

Reciprocal relations between growth factors suggest an overlapping pathway of secretion and activity.

Keywords

Salivary gland tumors VEGF EGF Saliva Angiogenesis VEGFR1

Effects of Selol 5% supplementation on tissue antioxidant enzyme levels and peroxidation marker in healthy mice

Posted by M Sochacka, M Remiszewska, P Suchocki, et al. on 2018-06-24 19:32:35

Abstract

Background

Selenium (Se) is an essential micronutrient for animals and humans used in the prevention or treatment of cancer. Selol is a mixture of selenitetriglycerides, containing Se(IV). It does not exhibit mutagenic activity and is less toxic than inorganic sodium selenite containing Se(IV). The antioxidant properties of the Selol were demonstrated using the blood of healthy animals. The aim of the study was to evaluate Selol as a Se supplement by determining the effect of its administration on the Se level and the antioxidant status in the tissues.

Methods

We examined the effect of long-term (28-day) Selol 5% supplementation on the activity of antioxidant enzymes, including the main selenoenzymes in healthy mice organs, such as liver, brain, lungs, and testis. Enzyme activities of the tissue homogenates and the concentration of malondialdehyde (MDA) as a biomarker of oxidative stress were measured using spectrophotometric methods. The selenium concentrations in the tissues were determined by inductively coupled plasma mass spectrometer (ICP-MS) as well.

Results

A significant increase in glutathione peroxidase, thioredoxin reductase, and glutathione S-transferase activity as well as the MDA concentration was observed in most of the studied tissues during the Selol 5% supplementation.

Conclusions

Long-term supplementation with the new Se (IV) compound - Selol 5% significantly affects the activity of antioxidant enzymes and the redox state in healthy mice organs. In the healthy population Selol 5% seems to be a promising new antioxidant compound.

Keywords

Selenium; Selol; Glutathione peroxidase; Thioredoxin reductase; Malondialdehyde

Dunnione protects against experimental cisplatin-induced nephrotoxicity by modulating NQO1 and NAD+ levels

Posted by N Rashtchizadeh, H Argani, L Roshangar, et al. on 2018-06-24 18:59:58

Abstract

Despite being an efficacious anticancer agent, the clinical utility of cisplatin is hindered by its cardinal side effects. This investigation aimed to appraise potential protective impact of dunnione, a natural naphthoquinone pigment with established NQO1 stimulatory effects, on cisplatin nephrotoxicity of rats. Dunnione was administered orally at 10 and 20 mg/kg doses for 4 d and a single injection of cisplatin was delivered at the second day. Renal histopathology, inflammatory/oxidative stress/apoptotic markers, kidney function, and urinary markers of renal injury were assessed. Dunnione repressed cisplatin-induced inflammation in the kidneys as indicated by decreased TNF-alpha/IL-1beta levels, and reduced nuclear phosphorylated NF-kB p65. This agent also obviated cisplatin-invoked oxidative stress as elucidated by decreased MDA/GSH levels and increased SOD/CAT activities. Dunnione, furthermore, improved renal histological deteriorations as well as caspase-3 activities and terminal deoxynucleotidyl transferase (TUNEL) positive cells, the indicators of apoptosis. Moreover, it up-regulated nuclear Nrf2 and cytosolic haeme-oxygenase-1 (HO-1) and NQO1 levels; meanwhile, promoted NAD+/NADH ratios followed by enhancing the activities of Sirt1 and PARP1; and further attenuated nuclear acetylated NF-kB p65. Dunnione additionally declined cisplatin-evoked retrogression in renal function and upraise in urinary markers of glomerular and tubular injury as demonstrated by decreased serum urea and creatinine with simultaneous reductions in urinary excretions of collagen type IV, podocin, cystatin C, and retinol-binding protein (RBP). Altogether, these findings offer dunnione as a potential protective agent against cisplatin-induced nephrotoxicity in rats.

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