Nardosinone was isolated as an enhancer of nerve growth factor (NGF) from Nardostachys chinensis. Nardosinone (0.1-100 microM) enhanced dibutyryl cyclic AMP (dbcAMP, 0.3 mM)- and staurosporine (10 nM)-induced neurite outgrowth from PC12D cells in a concentration-dependent manner, suggesting that Nardosinone enhances a downstream step of MAP kinase in the MAP kinase-dependent signaling pathway.
Nardosinone was isolated as an enhancer of nerve growth factor (NGF) from Nardostachys chinensis. Nardosinone (0.1-100 microM) enhanced dibutyryl cyclic AMP (dbcAMP, 0.3 mM)- and staurosporine (10 nM)-induced neurite outgrowth from PC12D cells in a concentration-dependent manner. Nardosinone enhances a downstream step of MAP kinase in the MAP kinase-dependent signaling pathway[3]. Nardosinone may reduce the motor and cognitive symptoms in the animal PD model by regulating DRD2 (Dopamine receptor D2) expression[4]. Pretreatment with nardosinone (25, 50, 100, and 200 μmol/L) could significantly inhibit the enlargement of cell surface area induced by AngII. The protective effects of nardosinone might be mediated by repressing the phosphorylation of related proteins in PI3K/Akt and MEK/ERK signaling pathways[5]. Nardosinone promotes cells proliferation and increases cells migration distance in a dose-dependent manner. Nardosinone also induces the selective differentiation of neural stem cells to neurons and oligodendrocytes, as indicated by the expression of microtubule-associated protein-2 and myelin basic protein, respectively. Nardosinone also increases the expression of phospho-extracellular signal-regulated kinase and phospho-cAMP response element binding protein during proliferation and differentiation[6].
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