Vaccinium bracteatum Thunb. Exerts Anti-Inflammatory Activity by Inhibiting NF-κB Activation in BV-2 Microglial Cells.
10.4062/biomolther.2015.205
- Author:
Seung Hwan KWON
1
;
Shi Xun MA
;
Yong Hyun KO
;
Jee Yeon SEO
;
Bo Ram LEE
;
Taek Hwan LEE
;
Sun Yeou KIM
;
Seok Yong LEE
;
Choon Gon JANG
Author Information
1. Department of Pharmacology, School of Pharmacy, Sungkyunkwan University, Suwon 16419, Republic of Korea. jang@skku.edu
- Publication Type:Original Article
- Keywords:
Vaccinium bracteatum Thunb;
Anti-inflammatory activity;
Nuclear factor-κB p65;
Lipopolysaccharide;
BV-2 microglial cells
- MeSH:
Cytokines;
Interleukin-1beta;
Interleukin-6;
Methanol;
Neurodegenerative Diseases;
Nitric Oxide;
Nitric Oxide Synthase;
Phosphorylation;
Prostaglandin-Endoperoxide Synthases;
Reactive Oxygen Species;
Tumor Necrosis Factor-alpha;
Up-Regulation;
Vaccinium*
- From:Biomolecules & Therapeutics
2016;24(5):543-551
- CountryRepublic of Korea
- Language:English
-
Abstract:
This study was designed to evaluate the pharmacological effects of Vaccinium bracteatum Thunb. methanol extract (VBME) on microglial activation and to identify the underlying mechanisms of action of these effects. The anti-inflammatory properties of VBME were studied using lipopolysaccharide (LPS)-stimulated BV-2 microglial cells. We measured the production of nitric oxide (NO), inducible NO synthase (iNOS), cyclooxygenase (COX)-2, prostaglandin E₂ (PGE₂), tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6) as inflammatory parameters. We also examined the effect of VBME on intracellular reactive oxygen species (ROS) production and the activity of nuclear factor-kappa B p65 (NF-κB p65). VBME significantly inhibited LPS-induced production of NO and PGE₂ and LPS-mediated upregulation of iNOS and COX-2 expression in a dose-dependent manner; importantly, VBME was not cytotoxic. VBME also significantly reduced the generation of the pro-inflammatory cytokines TNF-α, IL-1β, and IL-6. In addition, VBME significantly dampened intracellular ROS production and suppressed NF-κB p65 translocation by blocking IκB-α phosphorylation and degradation in LPS-stimulated BV2 cells. Our findings indicate that VBME inhibits the production of inflammatory mediators in BV-2 microglial cells by suppressing NF-κB signaling. Thus, VBME may be useful in the treatment of neurodegenerative diseases due to its ability to inhibit inflammatory mediator production in activated BV-2 microglial cells.
