Gua Lou Gui Zhi decoction suppresses LPS-induced activation of the TLR4/NF-κB pathway in BV-2 murine microglial cells

Hu,Haixia; Li,Zuanfang; Zhu,Xiaoqin; Lin,Ruhui; Lin,Jiumao; Peng,Jun; Tao,Jing; Chen,Lidian

doi:10.3892/ijmm.2013.1331

Gua Lou Gui Zhi decoction suppresses LPS-induced activation of the TLR4/NF-κB pathway in BV-2 murine microglial cells

Authors:
- Haixia Hu
- Zuanfang Li
- Xiaoqin Zhu
- Ruhui Lin
- Jiumao Lin
- Jun Peng
- Jing Tao
- Lidian Chen
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Affiliations: Key Laboratory of TCM Rehabilitation of the State Administration of Traditional Chinese Medicine, Fujian University of Traditional Chinese Medicine, Minhou Shangjie, Fuzhou, Fujian 350122, P.R. China, Fujian Rehabilitation Technology Engineering Center, Fujian University of Traditional Chinese Medicine, Minhou Shangjie, Fuzhou, Fujian 350122, P.R. China, MOE Key Laboratory of Traditional Chinese Medicine on Osteology and Traumatology and Exercise Rehabilitation, Fujian University of Traditional Chinese Medicine, Minhou Shangjie, Fuzhou, Fujian 350122, P.R. China, Fujian Key Laboratory of Exercise Rehabilitation, Fujian University of Traditional Chinese Medicine, Minhou Shangjie, Fuzhou, Fujian 350122, P.R. China
Published online on: April 5, 2013 https://doi.org/10.3892/ijmm.2013.1331
Pages: 1327-1332

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Abstract

Toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB) signaling-mediated neuroinflammation contributes to secondary brain damage in ischemic stroke; therefore, anti-inflammatory therapy via suppression of the TLR4/NF-κB pathway could be a promising strategy for the treatment of stroke and post-stroke disabilities. Gua Lou Gui Zhi decoction (GLGZD) has long been used in China to clinically treat dysfunction after stroke such as muscular spasticity, but the precise mechanisms are largely unknown. In the present study, we evaluated the anti-inflammatory effect of GLGZD and investigated the underlying molecular mechanisms using lipopolysaccharide (LPS)-stimulated BV-2 microglial cells as an in vitro inflammatory model of neural cells. We found that GLGZD inhibited the inflammatory response in microglial cells as it significantly reduced LPS-induced expression of pro-inflammatory nitric oxide, tumour necrosis factor-α, interleukin (IL)-6 and IL-1β in BV-2 cells, in a dose-dependent manner. In addition, GLGZD treatment significantly decreased the protein expression of TLR4 and myeloid differentiation factor 88, inhibited the phosphorylation of IκB and blocked the nuclear translocation of NF-κB in BV-2 cells, demonstrating its inhibitory effect on the activation of TLR4/NF-κB signaling. Collectively, our findings suggest that inhibition of the inflammatory response via suppression of the TLR4/NF-κB pathway may be one of the mechanisms through which GLGZD ameliorates the damage in ischemic cerebral tissues.

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