Lycopene mitigates β-amyloid induced inflammatory response and inhibits NF-κB signaling at the choroid plexus in early stages of Alzheimer's disease rats

The choroid plexus is able to modulate the cognitive function, through changes in the neuroinflammatory response and in brain immune surveillance. However, whether lycopene is involved in inflammatory responses at the choroid plexus in the early stages of Alzheimer's disease, and its molecular underpinnings are elusive. In this rat study, lycopene was used to investigate its protective effects on inflammation caused by beta-amyloid. We characterized the learning and memory abilities, cytokine profiles of circulating TNF-alpha, IL-1 beta and IL-6 beta in the serum and the expressions of Toll like receptor 4 and nuclear factor kappa B p65 mRNA and protein at the choroid plexus. The results showed that functional deficits of learning and memory in lycopene treatment groups were significantly improved compared to the control group without lycopene treatment in water maze test. The levels of serum TNF-alpha, IL-1 beta and IL-6 beta were significantly increased, and the expressions of TLR4 and NF-kappa B p65 mRNA and protein at the choroid plexus were up-regulated, indicating inflammation response was initiated following administration of A beta(1-42). After intragastric pretreatment with lycopene, inflammatory cytokines were significantly reduced and lycopene also reversed the A beta(1-42) induced up -regulation of TLR4 and NF-kappa B p65 mRNA and protein expressions at the choroid plexus. These results provided a novel evidence that lycopene significantly improved cognitive deficits and were accompanied by the attenuation of inflammatory injury via blocking the activation of NF-kappa B p65 and TLR4 expressions and production of cytokines, thereby endorsing its usefulness for diminishing beta-amyloid deposition in the hippocampus tissues. (C) 2017 Elsevier Inc. All rights reserved.