text: Catalpol inhibits LPS plus IFN-γ-induced inflammatory response in astrocytes primary cultures.
  A large body of evidence suggests that the inflammatory reaction plays an important role in the pathogenesis of neurodegenerative diseases. Our previous studies described the neuroprotective effects of catalpol in lipopolysaccharide (LPS)-induced inflammatory models, in which catalpol was shown to prevent mesencephalic neuron death and ameliorate cognitive ability animals. To further investigate the protective effect and underlying mechanism of catalpol, astrocytes were pretreated with low (0.1mM) and high dose (0.5mM) catalpol for 1h prior to LPS plus interferon-γ stimulation. Biochemical analyses showed that NO and ROS production and iNOS activity were significantly reduced by catalpol. Data at transcriptional level also demonstrated that catalpol potently attenuated gene expressions involved in inflammation, such as iNOS, COX-2 and TLR4. In addition, our exploration further revealed that the suppressive action of catalpol on inflammation was mediated via inhibiting nuclear factor-κB (NF-κB) activation. Collectively, these results suggest that catalpol can exert inhibitory effects on the inflammatory reaction in astrocytes and that inactivation of NF-κB could be the major determinant for its anti-inflammatory mechanism. Therefore, catalpol may potentially be a highly effective therapeutic agent in treating neurodegenerative diseases associated with inflammation.
entities.id: T10 T11 T12 T13 T14 T15 T16 T17 T18 T19 T1 T20 T2 T3 T4 T5 T6 T7 T8 T9
entities.type: CHEMICAL CHEMICAL GENE-N GENE-N GENE-Y GENE-Y GENE-Y GENE-Y GENE-Y GENE-N CHEMICAL GENE-Y CHEMICAL CHEMICAL CHEMICAL CHEMICAL CHEMICAL CHEMICAL CHEMICAL CHEMICAL
entities.text: catalpol Catalpol NF-κB NF-κB interferon-γ iNOS iNOS COX-2 TLR4 nuclear factor-κB catalpol IFN-γ catalpol catalpol catalpol catalpol catalpol NO catalpol catalpol