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Anti-inflammatory and anti-oxidative effects of 3-(naphthalen-2-yl(propoxy)methyl)azetidine hydrochloride on ?-amyloid-induced microglial activation.


ABSTRACT: We aimed to assess the anti-inflammatory and antioxidative properties of KHG26792, a novel azetidine derivative, in amyloid ? (A?)-treated primary microglial cells. KHG26792 attenuated the A?-induced production of inflammatory mediators such as IL-6, IL-1?, TNF-?, and nitric oxide. The levels of protein oxidation, lipid peroxidation, ROS, and NADHP oxidase enhanced by A? were also downregulated by KHG26792 treatment. The effects of KHG26792 against the A?-induced increases in inflammatory cytokine levels and oxidative stress were achieved by increasing the phosphorylation of Akt/ GSK-3? signaling and by decreasing the A?-induced translocation of NF-?B. Our results provide novel insights into the use of KHG26792 as a potential agent against A? toxicity, including its role in the reduction of inflammation and oxidative stress. Nevertheless, further investigations of cellular signaling are required to clarify the in vivo effects of KHG26792 against A?-induced toxicity. [BMB Reports 2017; 50(12): 634-639].

SUBMITTER: Yang SJ 

PROVIDER: S-EPMC5749910 | biostudies-literature | 2017 Dec

REPOSITORIES: biostudies-literature

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Anti-inflammatory and anti-oxidative effects of 3-(naphthalen-2-yl(propoxy)methyl)azetidine hydrochloride on β-amyloid-induced microglial activation.

Yang Seung-Ju SJ   Kim Jiae J   Lee Sang Eun SE   Ahn Jee-Yin JY   Choi Soo Young SY   Cho Sung-Woo SW  

BMB reports 20171201 12


We aimed to assess the anti-inflammatory and antioxidative properties of KHG26792, a novel azetidine derivative, in amyloid β (Aβ)-treated primary microglial cells. KHG26792 attenuated the Aβ-induced production of inflammatory mediators such as IL-6, IL-1β, TNF-α, and nitric oxide. The levels of protein oxidation, lipid peroxidation, ROS, and NADHP oxidase enhanced by Aβ were also downregulated by KHG26792 treatment. The effects of KHG26792 against the Aβ-induced increases in inflammatory cytoki  ...[more]

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