In the current study, we determined the effects of Ampelopsin (AMP) on the levels of proinflammatory cytokines (PICs, IL-1β, IL-6 and TNF-α), and products of oxidative stress 8-isoprostaglandin F2α (8-iso PGF2α, a product of oxidative stress); and 8-hydroxy-2'-deoxyguanosine (8-OHdG, a key biomarker of protein oxidation) in the hippocampus using a rat model of AD.
Interleukin-1β is a potent proinflammatory cytokine that plays a key role in the pathogenesis of the brain aging and diverse range of neurological diseases including Alzheimer's disease, Parkinson's disease, stroke and persistent pain.
All-trans retinoic acid cotreatment (1 mg/kg BW, i.p. daily) of DSS-treated mice (3% in drinking water for 7 days) alleviated colitis-associated weight loss, diarrheal phenotype, and induction of IL-1β and CXCL1 and a decrease in DRA mRNA and protein levels in the colon.
A dozen were shown to possess improved properties, among which inhibition of YO-PRO-1/TO-PRO-3 uptake and IL1β release upon BzATP activation of the receptor and dampening signs of DSS-induced colitis on mice, in comparison with reference antagonist GSK1370319A.
Our findings established a link between monocyte-like CD163-MNPs, IL-12, IL-1β and the detection of colonic memory IL-8-producing CD4+T cells, which might all contribute to UC pathogenesis.
The activation of A3AR by 2-Cl-IB-MECA significantly decreased TNF-α and IL-1β production and attenuated the NF-κB p65 activation in colonic tissues from patients with UC.
The hippocampus is particularly vulnerable to altered concentrations of the pro-inflammatory cytokine interleukin-1β (IL-1β), with elevated levels implicated in the aetiology of neurodegenerative disorders such as Alzheimer's and Parkinson's, and stress-related disorders such as depression.
We found that MI triggered NLRP3 inflammasome activation leading to conversion of interleukin-1β (IL-1β) and IL-18 into their active mature forms in the heart, which could expand the infarct size and drive cardiac dysfunction.
Cases had higher levels of IL-1Ra at all time-points leading up to first-time MI, and higher levels of IL-1Ra were associated with approximately 1.5-fold increased risk of MI, supporting the rationale to target IL-1 activation in order to reduce cardiovascular risk in PWH.
Recently, the CANTOS (Canakinumab Anti-Inflammatory Thrombosis Outcomes Study) showed the successful anti-inflammatory benefit of canakinumab, a monoclonal antibody targeting interleukin-1ß (IL-1ß) toward major cardiovascular events (MACE) in patients with a previous myocardial infarction (MI).
We hypothesized that TLMPs trigger inflammasome activation and IL-1β production in bronchial and alveolar epithelial cells to induce airway and lung inflammation.
Intratracheal instillation of nZnO intensively aggravated LPS-induced lung inflammation that was accompanied by enhanced expression of interleukin-1β, interleukin-6, monocyte chemotactic protein-1αand granulocyte-macrophage colony stimulating factor.
In the current report, we determined the effects of microRNA-155 (miR-155) on the levels of IL-1β, IL-6 and TNF-α, and their respective receptors in the hippocampus using a rat model of AD.
Moreover, apelin-13 inhibited microglia and astrocyte activation, reduced IL-1β and TNF-α expression and hippocampal BDNF/TrkB expression deficit in AD rats.
This study measured amyloid-beta (Aβ), interleukin-1 beta (IL-1β), and glial fibrillary acidic protein (GFAP) expression in the hippocampus of Alzheimer's disease (AD) rat models to elucidate the mechanism of anti-inflammatory effect of ginsenoside Rb1 in AD.
Furthermore, THS reduced mRNA expression of the proinflammatory cytokines, TNF-α, IL-6, and IL-1β and increased synapse-associated proteins (synaptophysin and postsynaptic density protein 95) in the hippocampus of AD mice.
The db mutation also reduced the cortical IL-1β mRNA level and IBA1 protein level in young AD mice, with no significant effect on the activation of microglia and astrocytes.
In the AD model group, the inhibition of PC12 cell growth was significantly increased, and the mRNA expression levels of IL‑1β, IL‑6, TNF‑α and MIF were also increased.
Increased expression of IL-1β and iron accumulation have been identified in microglial cells that cluster around amyloid plaques in AD mouse models and post-mortem brain tissues of AD patients.
Our data showed that SEO improved the cognitive ability of mice with Aβ<sub>1-42</sub> or lipopolysaccharides (LPS)-induced Alzheimer's disease (AD) and suppressed the production of tumor necrosis factor-a (TNF-a), interleukin-6 (IL-6), and interleukin-1β (IL-1β) in the hippocampus.