Open Access1,8-cineol attenuated Aβ25-35-induced neuron injury through inhibiting IL-6, IL-8 release and NF-κB expression
Author(s) -
Changliang Lu,
Lin Wang,
Shumei Wang,
Wanzhong Li,
LI Haijian,
Lichao Sun,
Wenzhen Shi,
Chunzhen Zhao
Publication year - 2019
Publication title -
journal of biomedical and pharmaceutical research
Language(s) - English
Resource type - Journals
eISSN - 2589-8752
pISSN - 2279-0594
DOI - 10.32553/jbpr.v8i1.567
Subject(s) - viability assay , lactate dehydrogenase , blot , mtt assay , chemistry , neuron , interleukin , cytokine , microbiology and biotechnology , cell , pharmacology , biology , biochemistry , immunology , enzyme , neuroscience , gene
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.