scholarly journals Effects of antihypertensive treatment on systemic inflammation, oxidative stress and proinflammatory cytokine levels

2020 ◽  
Vol 11 (4) ◽  
pp. 536-541
Author(s):  
T. V. Ashcheulova ◽  
N. N. Gerasimchuk ◽  
O. N. Kovalyova ◽  
K. N. Kompaniiets ◽  
O. V. Honchar
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Type I ◽  
Soluble Receptor ◽  
Tumour Necrosis Factor Α ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Hypertension in its origin is a heterogeneous and multisystemic disease. Evaluation of oxidative stress activity based on the level of 8-iso-PgF2α, proinflammatory activity based on tumour necrosis factor-α, its type I soluble receptor, and C-reactive protein levels is relevant for further understanding of pathogenesis of hypertension and improvement of the early diagnostics of heart failure. 186 hypertensive patients were observed during a 2-months course of treatment, aged 30 to 65 years. Serum levels of 8-iso-PgF2α (n = 34), tumour necrosis factor-α and its type I soluble receptor were determined by ELISA before and after course of treatment. C-reactive protein level was determined by biochemical method. The control group included 16 clinically healthy individuals, aged 27 to 55 years. Hypertensive patients enrolled into the study were randomized into three groups that received different protocols of combined anti-hypertensive therapy: I clinical group – а combination of bisoprolol and indapamid, II – а combination of lacidipine and candesartan, III – а combination of fosinopril sodium and hydrochlorothiazide. On the background of combined antihypertensive therapy, we observed favourable dynamics of 8-iso-PgF2α, tumour necrosis factor-α and its type I soluble receptor, and C-reactive protein levels. Taking into account the insignificance of the correlations revealed, a one-factor dispersion analysis was applied which allowed us to determine the influence of the grade and duration of hypertension on the dynamics of the studied parameters. It has been found that the grade of hypertension is related to an increase in TNF-α and 8-iso-PgF2α serum levels, but not in TNF-α type I soluble receptor, and the duration of hypertension is related to an increase in C-reactive protein, TNF-α and its type I soluble receptor levels, with no relation to the level of 8-iso-PgF2α. Thus, oxidative stress possibly promotes the activation of potentially damaging immune mechanisms mediated by proinflammatory cytokines, nonspecific inflammation and drives the further progression of lesions in the target organs.

Mediator effects of parameters of inflammation and neurogenesis from a N-acetyl cysteine clinical-trial for bipolar depression

2018 ◽  
Vol 30 (6) ◽  
pp. 334-341 ◽  
Author(s):  
Bruna Panizzutti ◽  
Chiara Bortolasci ◽  
Kyoko Hasebe ◽  
Srisaiyini Kidnapillai ◽  
Laura Gray ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Tumour Necrosis ◽  
Bipolar Depression ◽  
Tumour Necrosis Factor Α ◽  
C Reactive Protein ◽  
Open Label ◽  
Reactive Protein ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

AbstractObjectiveThis study aimed to explore effects of adjunctive treatment with N-acetyl cysteine (NAC) on markers of inflammation and neurogenesis in bipolar depression.MethodsThis is a secondary analysis of a placebo-controlled randomised trial. Serum samples were collected at baseline, week 8, and week 32 of the open-label and maintenance phases of the clinical trial to determine changes in interleukin (IL)-6, IL-8, IL-10, tumour necrosis factor-α (TNF-α), C-reactive protein (CRP) and brain-derived neurotrophic factor (BDNF) following adjunctive NAC treatment, and to explore mediation and moderator effects of the listed markers.ResultsLevels of brain-derived neurotrophic factor (BDNF), tumour necrosis factor-α (TNF-α), C-reactive protein (CRP), interleukins (IL) -6, 8, or 10 were not significantly changed during the course of the trial or specifically in the open-label and maintenance phases. There were no mediation or moderation effects of the biological factors on the clinical parameters.ConclusionThe results suggest that these particular biological parameters may not be directly involved in the therapeutic mechanism of action of adjunctive NAC in bipolar depression.

Differential effect of selective block of α2-adrenoreceptors on plasma levels of tumour necrosis factor-α, interleukin-6 and corticosterone induced by bacterial lipopolysaccharide in mice

1995 ◽  
Vol 144 (3) ◽  
pp. 457-462 ◽  
Author(s):  
G Haskó ◽  
I J Elenkov ◽  
V Kvetan ◽  
E S Vizi
Keyword(s):  
Tumour Necrosis Factor ◽  
Interleukin 6 ◽  
Plasma Levels ◽  
Tumour Necrosis ◽  
Endotoxin Shock ◽  
Bacterial Lipopolysaccharide ◽  
Tumour Necrosis Factor Α ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Abstract The effect of selective block of α2-adrenoreceptors on plasma levels of tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6) and corticosterone induced by bacterial lipopolysaccharide (LPS) was investigated in mice using ELISA and RIA. It was found that the LPS-induced TNF-α response was significantly blunted in mice pretreated with CH-38083, a novel and highly selective α2-adrenoreceptor antagonist (the α2/α1 ratio is >2000). In contrast, LPS-induced increases in both corticosterone and IL-6 plasma levels were further increased by CH-38083. Since it has recently been shown that the selective block of α2-adrenoreceptors located on noradrenergic axon terminals resulted in an increase in the release of noradrenaline (NA), both in the central and peripheral nervous systems, and, in our experiments, that propranolol prevented the effect of α2-adrenoreceptor blockade on TNF-α plasma levels induced by LPS, it seems likely that the excessive stimulation by NA of β-adrenoreceptors located on cytokine-secreting immune cells is responsible for this action. Since it is generally accepted that increased production of TNF-α is involved in the pathogenesis of inflammation and endotoxin shock on the one hand, and corticosterone and even IL-6 are known to possess anti-inflammatory properties on the other hand, it is suggested that the selective block of α2-adrenoreceptors might be beneficial in the treatment of inflammation and/or endotoxin shock. Journal of Endocrinology (1995) 144, 457–462

scholarly journals High blood soluble receptor p80 for tumour necrosis factor‐α is associated with erythropoietin resistance in haemodialysis patients

2001 ◽  
Vol 16 (9) ◽  
pp. 1838-1844 ◽  
Author(s):  
Akihiko Kato ◽  
Mari Odamaki ◽  
Takako Takita ◽  
Mitsuyoshi Furuhashi ◽  
Yukitaka Maruyama ◽  
...  
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Soluble Receptor ◽  
Tumour Necrosis Factor Α ◽  
Factor Α ◽  
Erythropoietin Resistance ◽  
Necrosis Factor

scholarly journals Intracellular NAD+ levels are associated with LPS-induced TNF-α release in pro-inflammatory macrophages

2016 ◽  
Vol 36 (1) ◽  
Author(s):  
Abbas Jawad Al-Shabany ◽  
Alan John Moody ◽  
Andrew David Foey ◽  
Richard Andrew Billington
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Inflammatory Cytokine ◽  
Bacterial Lipopolysaccharide ◽  
Tumour Necrosis Factor Α ◽  
Tnf Α ◽  
Factor Α ◽  
Inflammatory Macrophages ◽  
Inflammatory Macrophage ◽  
Necrosis Factor

Bacterial lipopolysaccharide induces changes in intracellular NAD+ levels in a pro-inflammatory, but not an anti-inflammatory, macrophage model that are correlated with the release of the pro-inflammatory cytokine tumour necrosis factor-α (TNF-α).

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