Exploring the association between interleukin-1β and its interacting proteins in Alzheimer’s disease

Xie, Lushuang; Lai, Yu; Lei, Fang; Liu, Sujuan; Liu, Ran; Wang, Ting‐Hua

doi:10.3892/mmr.2015.3183

Cited by 21 publications

(15 citation statements)

References 30 publications

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“…Evidence indicates that IL-1β expression is one of the most important neuropathological factors in ND, such as AD, being recognized as a central factor in neuroinflammation (Azizi and Mirshafiey, 2012;Xie et al, 2015). Second (Halle et al, 2008) the activation of the NLRP3 inflammasome is closely associated with caspase 1 activation and IL-1β release by Aβ-exposed microglia.…”

Section: Discussionmentioning

confidence: 99%

Neuroimmunomodulatory and Neuroprotective Effects of the Flavonoid Apigenin in in vitro Models of Neuroinflammation Associated With Alzheimer’s Disease

Dourado

Souza

Almeida

et al. 2020

Front. Aging Neurosci.

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Apigenin Modulates Glia and Protects Neurons apigenin reduced microglial activation, characterized by inhibition of proliferation (BrdU+ cells) and modulation of microglia morphology (Iba-1 + cells), and decreased the expression of the M1 inflammatory marker CD68. Moreover, as determined by RT-qPCR, inflammatory stimuli induced by IL-1β increased the mRNA expression of IL-6, IL-1β, and CCL5, and decreased the mRNA expression of IL-10. Contrary, after treatment with apigenin in inflammatory stimuli (IL-1β or LPS) there was a modulation of the mRNA expression of inflammatory cytokines, and reduced expression of OX42, IL-6 and gp130. Moreover, apigenin alone and after an inflammatory stimulus with IL-1β also induced the increase in the expression of brain-derived neurotrophic factor (BDNF), an effect that may be associated with anti-inflammatory and neuroprotective effects. Together these data demonstrate that apigenin presents neuroprotective and anti-inflammatory effects in vitro and might represent an important neuroimmunomodulatory agent for the treatment of neurodegenerative conditions.

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Section: Discussionmentioning

confidence: 99%

Neuroimmunomodulatory and Neuroprotective Effects of the Flavonoid Apigenin in in vitro Models of Neuroinflammation Associated With Alzheimer’s Disease

Dourado

Souza

Almeida

et al. 2020

Front. Aging Neurosci.

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“…IL1b and Mpo are inflammatory genes that are strongly upregulated in AD [23] . Additionally, increased serum levels of IL1b are used as a stage marker of the ongoing brain neurodegeneration between normal aging and AD [24,25] . Aβ fibrils also promote the release of the inflammatory cytokine IL1b, which can damage neurons and promote AD progression [26] .…”

Section: Discussionmentioning

confidence: 99%

Optimal Formula of Angelica sinensis Ameliorates Memory Deficits in β-amyloid Protein-induced Alzheimer’s Disease Rat Model

Wang

et al. 2022

CURR MED SCI

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Objective Angelica (A.) sinensis is used as a traditional medical herb for the treatment of neurodegeneration, aging, and inflammation in Asia. A. sinensis optimal formula (AOF) is the best combination in A. sinensis that has been screened to rescue the cognitive ability in β-amyloid peptide (Aβ25–35)-treated Alzheimer’s disease (AD) rats. The objective of this study was to investigate the effect of AOF on the learning and memory of AD rats as well as to explore the underlying mechanisms. Methods Male Wistar rats were infused with Aβ25–35 for AD model induction or saline (negative control). Five groups of AD rats were fed on AOF at 20, 40, or 80 mL/kg every day, donepezil at 0.9 mg/kg every day (positive control), or an equal volume of water (AD model) intragastrically once a day for 4 weeks, while the negative control rats were fed on water. The Morris water maze test was used to evaluate the cognitive function of the rats. The Aβ accumulation, cholinergic levels, and antioxidative ability were detected by ELISA. Additionally, the candidate mechanism was determined by gene sequencing and quantitative real-time polymerase chain reaction. Results The results showed that AOF administration significantly ameliorated Aβ25–35-induced memory impairment. AOF decreased the levels of amyloid-β precursor protein and Aβ in the hippocampus, rescued the cholinergic levels, increased the activity of superoxide dismutase, and decreased the malondialdehyde level. In addition, AOF inhibited the expression of IL1b, Mpo, and Prkcg in the hippocampus. Conclusion These experimental findings illustrate that AOF prevents the decrease in cognitive function and Aβ deposits in Aβ25–35-treated rats via modulating neuroinflammation and oxidative stress, thus highlighting a potential therapeutic avenue to promote the co-administration of formulas that act on different nodes to maximize beneficial effects and minimize negative side effects.

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“…2-Octenal, 2-hexenal, and 2,4-decadienal have shown to induce higher interleukin-1β (IL-1β) release, whereas alkanals such as hexanal, octanal, and decanal exhibited reduced release activities in human mononuclear cells [24,44]. IL-1β is known as a key component of proinflammatory cytokines and relates to the development and progression of many diseases (e.g., atherosclerosis, type II diabetes, rheumatoid arthritis, and neurogenerative diseases) [45,46]. Figure 5.…”

Section: Discussionmentioning

confidence: 99%

The Combination of Cigarette Smoking and Alcohol Consumption Synergistically Increases Reactive Carbonyl Species in Human Male Plasma

Mure

Tomono

Mure

et al. 2021

IJMS

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Cigarette smoking and alcohol consumption are major risk factors for lifestyle-related diseases. Although it has been reported that the combination of these habits worsens risks, the underlying mechanism remains elusive. Reactive carbonyl species (RCS) cause chemical modifications of biological molecules, leading to alterations in cellular signaling pathways, and total RCS levels have been used as a lipid peroxidation marker linked to lifestyle-related diseases. In this study, at least 41 types of RCS were identified in the lipophilic fraction of plasma samples from 40 subjects using liquid chromatography/electrospray ionization tandem mass spectrometry (LC/ESI-MS/MS). Higher levels of 10 alkanals, 5 trans-2-alkenals, 1 cis-4-alkenal, and 3 alkadienals were detected in the smoking/drinking group (N = 10) as compared to those with either habit (N = 10 each) or without both habits (N = 10) in the analysis of covariances adjusted for age and BMI. The levels of 3 alkanals, 1 trans-2-alkenal, 1 alkadienal, and 1 4-hydroxy-2-alkenal in the smoking/drinking group were significantly higher than those in the no-smoking/drinking and no-smoking/no-drinking groups. These results strongly indicate that the combination of cigarette smoking and alcohol drinking synergistically increases the level and variety of RCS in the circulating blood, and may further jeopardize cellular function.

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Exploring the association between interleukin-1β and its interacting proteins in Alzheimer’s disease

Cited by 21 publications

References 30 publications

Neuroimmunomodulatory and Neuroprotective Effects of the Flavonoid Apigenin in in vitro Models of Neuroinflammation Associated With Alzheimer’s Disease

Neuroimmunomodulatory and Neuroprotective Effects of the Flavonoid Apigenin in in vitro Models of Neuroinflammation Associated With Alzheimer’s Disease

Optimal Formula of Angelica sinensis Ameliorates Memory Deficits in β-amyloid Protein-induced Alzheimer’s Disease Rat Model

The Combination of Cigarette Smoking and Alcohol Consumption Synergistically Increases Reactive Carbonyl Species in Human Male Plasma

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