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2-cyclohexylamino-5,8-dimethoxy-1,4-naphthoquinone inhibits LPS-induced BV2 microglial activation through MAPK/NF-kB signaling pathways

AIMS: To verify the effects of several 5,8-dimethoxy-1,4-naphthoquinone (DMNQ) derivatives on LPS-induced NO production, cellular ROS levels and cytokine expression in BV-2 microglial cells. MAIN METHODS: An MTT assay and FACS flow cytometry were performed to assess the cellular viability and apopto...

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Detalles Bibliográficos
Autores principales: Sun, Hu-Nan, Shen, Gui-Nan, Jin, Yong-Zhe, Jin, Yu, Han, Ying-Hao, Feng, Li, Liu, Lei, Jin, Mei-Hua, Luo, Ying-Hua, Kwon, Tea-Ho, Cui, Yu-Dong, Jin, Cheng-Hao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4971128/
https://www.ncbi.nlm.nih.gov/pubmed/27512726
http://dx.doi.org/10.1016/j.heliyon.2016.e00132
Descripción
Sumario:AIMS: To verify the effects of several 5,8-dimethoxy-1,4-naphthoquinone (DMNQ) derivatives on LPS-induced NO production, cellular ROS levels and cytokine expression in BV-2 microglial cells. MAIN METHODS: An MTT assay and FACS flow cytometry were performed to assess the cellular viability and apoptosis and cellular ROS levels, respectively. To examine the expression of pro-inflammatory cytokines and cellular signaling pathways, semi-quantitative RT-PCR and Western blotting were also used in this study. KEY FINDINGS: Among the six newly synthesized DMNQ derivatives, 2-cyclohexylamino-5,8-dimethoxy-1,4-naphthoquinone (R6) significantly inhibited the NO production, cellular ROS levels and the cytokines expression in BV-2 microglial cells, which stimulated by LPS. Signaling study showed that compound R6 treatment also significantly down-regulated the LPS-induced phosphorylation of MAPKs (ERK, JNK and p38) and decreased the degradation of IκB-α in BV2 microglial cells. SIGNIFICANCE: Our findings demonstrate that our newly synthesized compound derived from DMNQ, 2-cyclohexylamino-5,8-dimethoxy-1,4-naphthoquinone (R6), might be a therapeutic agent for the treatment of glia-mediated neuroinflammatory diseases.