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.
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.
Further, a significant increased expression of cleaved caspase-1 and IL-1β, the products of inflammasome activation, was detected in the cortex of AD brains.
Increased concentrations of interleukin 1 (IL-1) in the cerebrospinal fluid and serum of patients with Alzheimer disease (AD) reduced phagocytic capacity point to an inflammatory activation of mononuclear phagocytes in AD.
Importantly, CTSB activity, IL-1β levels and malondialdehyde (MDA) were remarkably elevated in plasma of AD patients compared to healthy controls, while glutathione was significantly lower than healthy controls.
Brain inflammation including increases in inflammatory cytokines such as IL-1β is widely believed to contribute to the pathophysiology of Alzheimer's disease.
The results showed that the hippocampal and serum levels of ROS, nitrite, TNF-α, and IL-1β were significantly higher in the AD animals along with increased chromatolysis and impairments of memory.
Here we studied the effect of amyloid beta-peptides (Aβ), interleukin 1-beta (IL-1β), and CSF from AD, Lewy body dementia (LBD) or subjective cognitive impairment (SCI) patients on the NGF overproducing cell line NGC-0295.