Inhibition of Lipopolysaccharide-Induced Proinflammatory Responses by Buddleja officinalis Extract in BV-2 Microglial Cells via Negative Regulation of NF-κB and ERK1/2 Signaling

Molecules

Won-Jun Oh²  Uhee Jung¹  Hyun-Soo Eom²  Hee-June Shin² 

[1] Radiation Biotechnology Research Division, Advanced Radiation Technology Institute, Korea Atomic Energy Research Institute (KAERI), 1266 Sinjeong-dong Jeongeup-si, Jeonbuk 580-185, Korea;

关键词: Buddleja officinalis;    neuroinflammation;    microglia;    NF-κB;    ERK1/2;   

DOI  :  10.3390/molecules18089195

来源: mdpi

【 摘 要 】

Buddleja officinalis has been traditionally used in the supportive treatment of inflammatory and neuronal diseases in Korea and China. Although several reports have shown the anti-inflammatory effects of Buddleja officinalis, the anti-neuroinflammatory effect has remained unclear. In this study, we aimed to investigate the inhibitory effects of flower buds of B. officinalis Maximowicz water extract (BOWE) on LPS-induced inflammatory processes in BV-2 microglial cells. BOWE dose-dependently inhibited the production of nitric oxide as well as iNOS mRNA expression. Moreover, BOWE prevented IL-1β and IL-6 mRNA expression. However, BOWE had no effect on LPS-induced COX-2 or TNF-α mRNA expression. The extract also had no effect on LPS-stimulated p38 MAPK, JNK, and c-Jun phosphorylation, whereas ERK1/2 phosphorylation was strongly inhibited by BOWE. BOWE also inhibited the LPS-induced degradation of IκB-α, and LPS-induced phosphorylation of p65 NF-κB protein. These data indicate that BOWE inhibited the nitric oxide production and pro-inflammatory gene expression in BV-2 microglial cells, possibly through a negative regulation of the NF-κB and ERK1/2 pathways. Further identification of the direct target molecule(s) of BOWE is required to support its use as an anti-neuroinflammatory agent against the neurodegenerative disorders.

【 授权许可】

CC BY   
© 2013 by the authors; licensee MDPI, Basel, Switzerland.