Anti-neuro-inflammatory effects of Nardostachys chinensis in lipopolysaccharide-and lipoteichoic acid-stimulated microglial cells.
10.3724/SP.J.1009.2016.00343
- Author:
Sun Young PARK
1
;
Young Hun KIM
1
;
Geuntae PARK
2
,
3
Author Information
1. Bio-IT Fusion Technology Research Institute, Pusan National University, Busan, Korea.
2. Bio-IT Fusion Technology Research Institute, Pusan National University, Busan, Korea
3. Department of Nanomaterials Engineering, Pusan National University, Busan, Korea. Electronic address: gtpark@pusan.ac.kr.
- Publication Type:Journal Article
- Keywords:
Anti-inflammation;
Heme oxygenase-1;
Lipopolysaccharide;
Lipoteichoic acid;
Nardostachys chinensis
- MeSH:
Anti-Inflammatory Agents;
pharmacology;
Cell Line;
Heme Oxygenase-1;
genetics;
immunology;
Humans;
Lipopolysaccharides;
adverse effects;
Microglia;
cytology;
drug effects;
immunology;
Mitogen-Activated Protein Kinases;
genetics;
immunology;
NF-kappa B;
genetics;
immunology;
Nardostachys;
chemistry;
Neuroprotective Agents;
pharmacology;
Plant Extracts;
pharmacology;
Teichoic Acids;
adverse effects
- From:
Chinese Journal of Natural Medicines (English Ed.)
2016;14(5):343-353
- CountryChina
- Language:English
-
Abstract:
Excessive microglial cell activation is related to the progression of chronic neuro-inflammatory disorders. Heme oxygenase-1 (HO-1) expression mediated by the NFE2-related factor (Nrf-2) pathway is a key regulator of neuro-inflammation. Nardostachys chinensis is used as an anti-malarial, anti-nociceptive, and neurotrophic treatment in traditional Asian medicines. In the present study, we examined the effects of an ethyl acetate extract of N. chinensis (EN) on the anti-neuro-inflammatory effects mediated by HO-1 up-regulation in Salmonella lipopolysaccharide (LPS)- or Staphylococcus aureus lipoteichoic acid (LTA)-stimulated BV2 microglial cells. Our results indicated that EN suppressed pro-inflammatory cytokine production and induced HO-1 transcription and translation through Nrf-2/antioxidant response element (ARE) signaling. EN markedly inhibited LPS- and LTA-induced activation of nuclear factor-kappa B (NF-κB) as well as phosphorylation of mitogen-activated protein kinases (MAPKs) and signal transducer and activator of transcription (STAT). Furthermore, EN protected hippocampal HT22 cells from indirect neuronal toxicity mediated by LPS- and LTA-treated microglial cells. These results suggested that EN impairs LPS- and LTA-induced neuro-inflammatory responses in microglial cells and confers protection against indirect neuronal damage to HT22 cells. In conclusion, our findings indicate that EN could be used as a natural anti-neuro-inflammatory and neuroprotective agent.
