Biomol Ther.
2018 Mar;26(2):210-217. 10.4062/biomolther.2018.008.
Synthetic 3′,4′-Dihydroxyflavone Exerts Anti-Neuroinflammatory Effects in BV2 Microglia and a Mouse Model
- Affiliations
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- 1Department of Life and Nanopharmaceutical Sciences, Graduate School, Kyung Hee University, Seoul 02447, Republic of Korea.
- 2Department of Pharmacy, College of Pharmacy, Kyung Hee University, Seoul 02447, Republic of Korea. kimnj@khu.ac.kr
- 3Department of Pharmaceutical Science, College of Pharmacy, Kyung Hee University, Seoul 02447, Republic of Korea.
- 4Department of Oriental Pharmaceutical Science, College of Pharmacy, Kyung Hee University, Seoul 02447, Republic of Korea.
- KMID: 2429061
- DOI: http://doi.org/10.4062/biomolther.2018.008
Abstract
- Neuroinflammation is an immune response within the central nervous system against various proinflammatory stimuli. Abnormal activation of this response contributes to neurodegenerative diseases such as Parkinson disease, Alzheimer's disease, and Huntington disease. Therefore, pharmacologic modulation of abnormal neuroinflammation is thought to be a promising approach to amelioration of neurodegenerative diseases. In this study, we evaluated the synthetic flavone derivative 3"²,4"²-dihydroxyflavone, investigating its anti-neuroinflammatory activity in BV2 microglial cells and in a mouse model. In BV2 microglial cells, 3"²,4"²-dihydroxyflavone successfully inhibited production of chemokines such as nitric oxide and prostaglandin E2 and proinflammatory cytokines such as tumor necrosis factor alpha, interleukin 1 beta, and interleukin 6 in BV2 microglia. It also inhibited phosphorylation of mitogen-activated protein kinase (MAPK) and nuclear factor (NF)-κB activation. This indicates that the anti-inflammatory activities of 3"²,4"²-dihydroxyflavone might be related to suppression of the proinflammatory MAPK and NF-κB signaling pathways. Similar anti-neuroinflammatory activities of the compound were observed in the mouse model. These findings suggest that 3"²,4"²-dihydroxyflavone is a potential drug candidate for the treatment of microglia-related neuroinflammatory diseases.
Keyword
MeSH Terms
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Animals
Central Nervous System
Chemokines
Cytokines
Dinoprostone
Huntington Disease
Interleukin-1beta
Interleukin-6
Mice*
Microglia*
Neurodegenerative Diseases
Nitric Oxide
Parkinson Disease
Phosphorylation
Protein Kinases
Tumor Necrosis Factor-alpha
Chemokines
Cytokines
Dinoprostone
Interleukin-1beta
Interleukin-6
Nitric Oxide
Protein Kinases
Tumor Necrosis Factor-alpha
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