Sentences with phrase «of tumour necrosis factor»

In this study scientists fed mice just low doses of sulforaphane and found that there was significant inhibition of tumour necrosis factor alpha (TNF - a), which is one of the main players in inflammation.

Modulatory influence of unsaturated fatty acids on the biology of tumour necrosis factor - alpha

Enhanced monocyte binding to human cytomegalovirus - infected syncytiotrophoblast results in increased apoptosis via the release of tumour necrosis factor alpha.

Not exact matches

Researchers led by David Wallach of the Weizmann Institute of Science in Rehovot looked more closely at a receptor called p55, which binds to a suicide - promoting cytokine called tumour necrosis factor (TNF).

Such genes might include those for various cytokines — substances produced by cells of the immune system — such as tumour necrosis factor, interleukins and interferons.

It is mediated by the inflammatory cytokines interleukin - 1 and tumour - necrosis factor, both of which are produced in high amounts following sustained activation of Toll - like receptor 4 by LPS.

Abbreviations: ASC, apoptosis - associated speck - like protein containing a caspase - recruitment domain; ATM, adipose - tissue - resident macrophage; BAT, brown adipose tissue; CCR2, CC chemokine receptor 2; CHOP, C / EBP (CCAAT / enhancer - binding protein)- homologous protein; DHA, docosahexaenoic acid; EPA, eicosapentaenoic acid; ER, endoplasmic reticulum; GPCR, G - protein - coupled receptor; HIF, hypoxia - inducible factor; IFNγ, interferon γ; IKK, inhibitor of nuclear factor κB kinase; IL, interleukin; IRS - 1, insulin receptor substrate - 1; JNK, c - Jun N - terminal kinase; LDL, low - density lipoprotein; Ldlr, LDL receptor; LXR, liver X receptor; MCP - 1, monocyte chemoattractant protein 1; miRNA, microRNA; mTOR, mammalian target of rapamycin; NAFLD, non-alcoholic fatty liver disease; NF - κB, nuclear factor κB; NLRP3, NLR (nucleotide - binding - domain - and leucine - rich - repeat - containing) family, pyrin - domain - containing 3; oxLDL, oxidized LDL; PKR, double - stranded RNA - dependent protein kinase; PPAR, peroxisome - proliferator - activated receptor; STAT6, signal transducer and activator of transcription 6; SVF, stromal vascular fraction; TLR, Toll - like receptor; TNFα, tumour necrosis factor α; UPR, unfolded protein response; WAT, white adipose tissue

One theory proposes that once the storage capacity of subcutaneous adipose tissue (SAT) depots is exceeded under conditions of energy excess, either as a result of impaired expandability and / or excessive hypertrophic growth, fat deposition within visceral depots and non-adipose tissues including the liver, skeletal muscle and pancreas can ensue.93 This can subsequently lead to the development of systemic IR and a series of associated cardiometabolic disorders including dyslipidaemia, dysglycaemia, hyperinsulinaemia and hypertension.3 Expression of pro-inflammatory mediators including interleukins 1 (IL - 1), 6 (IL - 6), tumour necrosis factor alpha (TNF - α) and resistin, are also increased which can further potentiate IR and promote atherosclerosis.

Concentrations of inflammatory chemicals like tumour necrosis factor - alpha (TNF - a) fell, as did thiobarbituric acid reactive substances, a family of free radicals.

The scientists found that feeding the rats fluoride substantially increased levels of two pro-inflammatory cytokines called tumour necrosis factor alpha (TNF - a) and resistin.

For example, KBs were recently reported to act as neuroprotective agents by raising ATP levels and reducing the production of reactive oxygen species in neurological tissues, 80 together with increased mitochondrial biogenesis, which may help to enhance the regulation of synaptic function.80 Moreover, the increased synthesis of polyunsaturated fatty acids stimulated by a KD may have a role in the regulation of neuronal membrane excitability: it has been demonstrated, for example, that polyunsaturated fatty acids modulate the excitability of neurons by blocking voltage-gated sodium channels.81 Another possibility is that by reducing glucose metabolism, ketogenic diets may activate anticonvulsant mechanisms, as has been reported in a rat model.82 In addition, caloric restriction per se has been suggested to exert neuroprotective effects, including improved mitochondrial function, decreased oxidative stress and apoptosis, and inhibition of proinflammatory mediators, such as the cytokines tumour necrosis factor - α and interleukins.83 Although promising data have been collected (see below), at the present time the real clinical benefits of ketogenic diets in most neurological diseases remain largely speculative and uncertain, with the significant exception of its use in the treatment of convulsion diseases.

Another is local inflammation which is an increased production of what are called cytokines, like tumour necrosis factor for example.

Before weight loss, plasma tumour necrosis factor - alpha was above the detectable limits of the assay in 11 (42 %) of the dogs; after weight loss, only 3 dogs (12 %) had these high levels (P = 0.016)(German et al. 2009).