Abstract
Objective: To explore the protective effect of 1,8-cineol against Amyloid beta25-35 ( Aβ25-35)-induced cell injury in primary rat cortical neurons.
 Methods: Primary rat cortical neurons were cultured in vitro, treated with different concentrations of Aβ25-35 (2.5, 5, 10 20, 40 μM) and 1,8-cineol (1, 3, 10 μM). Cell viability of neuronal cells were detected by MTT assay and cell death were detected by lactate dehydrogenase release (LDH). The production of IL-6 and IL-8 in the supernatant were measured by ELISA assay kits. NF-κB protein expression was detected by Western blotting.
 Results: In primary cultured neurons, Aβ25-35 concentration dependently reduced cell viability and increased LDH release. 1,8-cineol with concentrations of 3 and 10 μM protected neuronal cells against Aβ25-35 induced cell injury for 24 h. 3 and 10 μM of 1,8-cineol also significantly decreased the levels of IL-6 and IL-8 cytokine production in the supernatant. Increased NF-κB expression was also significantly reduced by 1,8-cineol treatment evaluated by Western blotting.
 Conclusions: Our results revealed a protective effect of 1,8-cineol on Aβ25-35 induced neuron injury through inhibition of IL-6, IL-8 production and NF-κB expression.
Highlights
Amyloid beta (Aβ), which aggregate into oligomers in neurons, play a critical role in the pathogenesis of Alzheimer’s disease (AD)
In primary cultured neurons, Aβ25-35 concentration dependently reduced cell viability and increased lactate dehydrogenase release (LDH) release. 1,8-cineol with concentrations of 3 and 10 μM protected neuronal cells against Aβ25-35 induced cell injury for 24 h. 3 and 10 μM of 1,8-cineol significantly decreased the levels of IL-6 and IL-8 cytokine production in the supernatant
Our results revealed a protective effect of 1,8-cineol on Aβ25-35 induced neuron injury through inhibition of IL-6, IL-8 production and nuclear factor-κB (NF-κB) expression
Summary
Amyloid beta (Aβ), which aggregate into oligomers in neurons, play a critical role in the pathogenesis of Alzheimer’s disease (AD). Increasing evidence demonstrated that Aβ toxicity induced neurotoxicity in the cerebral cortex and hippocampus in vitro and in vivo, Chunzhen Zhao et al, Journal of Biomedical and Pharmaceutical Research resulting in neuronal apoptosis and cognitive dysfunction (Sowade et al 2017; Kim et al 2014; Robert et al 2015). Mainly composed of Aβ peptide, were found in AD patients brains, contributing to inflammatory responses (Vukic et al 2009). Deposits of Aβ in AD patients brain induced inflammation, leading to secretion of proinflammatory cytokines such as TNF-α and IL-8 (Hanzel et al 2014). The inflammatory pathway was further accelerated by nuclear factor-κB (NF-κB) activation, which translocated from the cytoplasm to the nucleus binding to its specific target genes including those involved in the inflammatory response (Srinivasa et al 2015)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
