摘要
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-?B) 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.
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 ofN. 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-r,B） 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.
基金
supported by the Basic Science Research Program through the National Research Foundation of Korea(NRF)funded by the Ministry of Education,Science,and Technology(2015R1D1A1A01059450)
the Ministry of Trade,Industry,and Energy(MOTIE)and the Korea Institute for Advancement of Technology(KIAT)through the Promoting Regional Specialized Industry Program(R0004422)
