scholarly journals Can coenzyme Q10 supplementation effectively reduce human tumour necrosis factor-α and interleukin-6 levels in chronic diseases? Protocol for a systematic review and meta-analysis of randomised controlled trials

BMJ Open ◽  
2017 ◽  
Vol 7 (10) ◽  
pp. e016841 ◽  
Author(s):  
Farnaz Farsi ◽  
Javad Heshmati ◽  
Leila Janani ◽  
Pardis Irandoost ◽  
Naeimeh Mesri Alamdari ◽  
...  
Keyword(s):  
Systematic Review ◽  
Coenzyme Q10 ◽  
Interleukin 6 ◽  
Tumour Necrosis ◽  
Meta Analysis ◽  
Tumour Necrosis Factor Α ◽  
Tnf Α ◽  
Randomised Controlled ◽  
Factor Α ◽  
Necrosis Factor

IntroductionInflammation, as a critical factor, can cause numerous chronic diseases by creating various proinflammatory cytokines. Coenzyme Q10 (CoQ10) can potentially exert an anti-inflammatory agent; in turn, this agent can reduce the systemic inflammatory response. The aims of this study are to conduct a comprehensive systematic review and a meta-analysis for the determination of the CoQ10 efficacy on the changes in serum interleukin-6 (IL-6) and the tumour necrosis factor-α (TNF-α) levels in unhealthy subjects.Method and analysisWe will conduct an electronic search for articles published between January 1990 and January 2017 using a prespecified search strategy in MEDLINE, SCOPUS, EMBASE, CENTRAL and Web of Science.Our search will focus only on randomised controlled clinical trials in unhealthy subjects that employ either a parallel or a crossover design; this search will involve concurrent control groups. The primary outcomes of the literature are to determine the CoQ10 efficacy on the changes in the serum IL-6 and the TNF-α levels in unhealthy subjects. Secondary outcomes such as body mass index, serum adiponectin and high-sensitivity C-reactive protein levels, lipid profile and the heterogeneity assessment of the primary studies will be evaluated. The stages of screen articles, the extracts of relevant data and the assessment of study quality using the Cochrane risk of bias tool will be conducted independently by the two reviewers. Any disagreement will be resolved by discussion with a third person. If the number of eligible studies is sufficient, we will carry out a meta-analysis according to both outcomes.Ethics and disseminationThis study is the protocol for a systematic review and no ethics approval is needed. The findings from the full systematic review will be published in a peer-reviewed journal, and they will also be exhibited at national/international academic and clinical conferences.Trial registration numberCRD42016052200.

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 Role of soluble gp130 in the tumour necrosis factor-α expression and its production by peripheral blood mononuclear cells

2003 ◽  
Vol 12 (6) ◽  
pp. 355-359
Author(s):  
E. Jablonskaca ◽  
W. Puzewska ◽  
M. Marcinczyk ◽  
J. Jablonski
Keyword(s):  
Tumour Necrosis Factor ◽  
Interleukin 6 ◽  
Peripheral Blood ◽  
Tumour Necrosis ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tumour Necrosis Factor Α ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor ◽  
Soluble Gp130

Background:In our previous study we found that rhsIL-6R, along with recombinant human interleukin-6, plays a regulatory role in the immune response by modulating the tumour necrosis factor-α (TNF-α) expression and its production by peripheral blood mononuclearcells (PBMC). We also suggested that sIL-6R with IL-6 secreted by human PMN (neutrophils) influenced the TNF-α expression and its production by autologous PBMC.Aims:Since soluble gp130 (sgp130) is a natural inhibitor for sIL-6R/interleukin-6 responses, in the present study we estimated an effect of exogenous recombinant human sgp130 and sgp130 secreted by PMN on the TNF-α expression and its production by PBMC.Methods:Cells were isolated from whole blood of healthy persons. The PMN were cultured in 96-well plates for 1 h at 37°C in a humidified incubator with 5% CO2. After the incubation, the culture supernatant of PMN was removed and added to the PBMC. PBMC were incubated for 1 h at 37°C in the same conditions. Cytoplasmic protein fractions of PMN and, for comparative purpose of PBMC, were analysed for presence of sgp130 by western blotting with the use of monoclonal antibody capable of detecting this protein. In the culture supernatants of PMN we examined the concentrations of sgp130 by human enzyme-linked immunosorbent assay. TNF-α was measured at the protein levels as well as the mRNA levels.Results and conclusions:The present results revealed that exogenous recombinant human sgp130 modulates the TNF-α expression and production by PBMC. In contrast, we did not find any effect of sgp130 secreted by PMN on the TNF-α expression and its production by autologous PBMC.

scholarly journals A systematic review and meta-analysis of biological treatments targeting tumour necrosis factor α for sciatica

2013 ◽  
Vol 22 (9) ◽  
pp. 1921-1935 ◽  
Author(s):  
Nefyn H. Williams ◽  
Ruth Lewis ◽  
Nafees Ud Din ◽  
Hosam E. Matar ◽  
Deborah Fitzsimmons ◽  
...  
Keyword(s):  
Systematic Review ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Meta Analysis ◽  
Tumour Necrosis Factor Α ◽  
Biological Treatments ◽  
Factor Α ◽  
Necrosis Factor
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