Cytokines neuroinflammatory reaction to the action of homoaggregatic and liposomal forms of b-amyloid 1-40 in rats

Vv, Sokolik; Maltsev, Alexander V.

doi:10.18097/pbmc20156103373

Cited by 4 publications

(2 citation statements)

References 22 publications

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“…However, in the cerebral cortex of these rats activation of inflammation reaction was also featured, albeit to a lesser extent. This result confirms our previous research, in which it was shown that homoaggregates of Аβ40_Human introduction into the cerebral cortex of rats causes more cytokine response in that part of the brain of rats in comparison with the situation in hippocampus [74].…”

Section: Cytokines Changes In Chronic Neuroinflammation Induced Homoasupporting

confidence: 92%

Anti-Cytokine Activity of Curcumin and Its Binding to a Fragment of AβPP

Sokolik¹,

Карпов

Samofalova

et al. 2016

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Since it has been shown that Alzheimer's disease is accompanied by higher peripheral concentrations of cytokines, we focused on the correction of chronic inflammation causing Aβ excess and aggregation what should have a positive impact. Proinflammatory cytokines action is realized by NF-κB intracellular signals. Curcumin can inhibit activation of the proinflammatory transcription factor NF-κB and is able to be mounted in the amyloid-β fibrils and encourage their disaggregation. To study the influence of anti-inflammatory effect of curcumin and its ability to model complexes with a fragment of AβPP. Investigation was carried out on rats with model of Alzheimer's disease using nasal therapy with curcumin Concentration of cytokines in cerebral cortex, hippocampus and blood serum, and indicators of conditioned active escape reflex were determined in this study. Methods of molecular dynamics and docking were used to examine the interactions of curcumin with fragment of AβPP. Аβ42_Human in the hippocampus of rats provoked chronic neuroinflammation specifically and primarily at the injection site. Curcumin performance revealed specific depressing effect on cytokines in the cerebral cortex and in the hippocampus it appeared similar to the above, but of lower level. Anti-inflammatory activity of curcumin led to the recovery of memory parameters. Analysis of restriction sites of AβPP has shown that position of curcumin in Site II is energetically more favorable for binding. Our suggestion that curcumin is an effective anti-cytokine factor was confirmed by experimental results obtained in vivo and explain the mechanism describing its effect on NF-κB Curcumin doesn't block the excision Aβ but binding with its hydrophobic region.

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Section: Cytokines Changes In Chronic Neuroinflammation Induced Homoasupporting

confidence: 92%

Anti-Cytokine Activity of Curcumin and Its Binding to a Fragment of AβPP

Sokolik¹,

Карпов

Samofalova

et al. 2016

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“…Yet recent studies have demonstrated trophic [9] properties of AβPP (antimicrobial, in particular), that served as basis for its comparison with other antimicrobial peptides (defensins, histatins, and cathelicidins) and attribution to brain's innate immune system [10]. We have proved [11] the role of chronic inflammation in initiation of amyloidosis, and the involvement of cytokines and Aβ in inflammatory response to toxic effects of Aβ-aggregates.…”

Section: Abstract: Curcumin β-Amyloid Peptides 40 and 42 (Aβ mentioning

confidence: 90%

Effect of curcumin on accumulation in mononuclear cells and secretion in incubation medium of А?(40) and cytokines under local excess of А?(42)-homoaggregates

Sokolik¹,

Shulga²

2016

Ukr.Biochem.J.

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The aim of the work was to investigate accumulation of endogenous Aβ40 and cytokines (IL-1β, TNFα, IL-6, IL-10) in mononuclear cells and their secretion into incubation medium under Aβ42-aggregates’ toxicity and anti-inflammatory effects of curcumin. Mononuclear cells were isolated in Ficoll-Urografin density gradient from venous blood of healthy donors, resuspended and used for testing of homoaggregates of Aβ42 (15 nM), curcumin (54 pM) and their combinations on various timescales (0, 1, 2, 3, 6 and 24 hours). Endogenous Aβ40 and cytokines were detected in mononuclear cells and (separately) in incubation medium by ELISA. We demonstrated for the first time that homoaggregates of Aβ42 cause rapid accumulation of endogenous Aβ40 in mononuclear cells and accelerate its secretion into incubation medium. We found increased concentration of TNFα after 3 hours of incubation, and no changes in IL-1β concentration due to secretion of these pro-inflammatory factors into incubation medium. The concentrations of IL-6 in mononuclear cells were increased under effects of Aβ42 homoaggregates, and it was being secreted profoundly into incubation medium. Aβ42 did not affect IL-10 secretion, yet caused an increase in its intracellular concentration after 1 hour of incubation, which was subsequently suppressed. Curcumin prevented the increase in Aβ40 concentration in mononuclear cells and significantly decreased its secretion resulting from Aβ42 toxicity. Curcumin negated the activating effect of Aβ42 on pro-inflammatory cytokines, starting immediately for IL-1β and on 3-6 hours for TNFα, which resulted in decreased extracellular concentrations of these cytokines. The polyphenol also potentiated replenishing of intracellular IL-6 and IL-10 concentrations and their secretion into incubation medium.

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