Catalpol attenuates nitric oxide increase via ERK signaling pathways induced by rotenone in mesencephalic neurons.

Catalpol has been shown to rescue neurons from kinds of damage in vitro and in vivo in previous reports. However, the effect of catalpol on the nitric oxide (NO) system via MAPKs signaling pathway of mesencephalic neurons largely remains to be verified. The current study examined that whether catalpol modulated NO and iNOS increase by rotenone in primary mesencephalic neurons and investigated its underlying signaling pathways. Present results indicated that catalpol inhibited primary mesencephalic neurons from apoptosis by morphological assay, immunocytochemistry and flow cytometric evaluation. Moreover, the ERK signaling pathway plays an important role in NO-mediated degeneration of neuron. The current results suggest that catalpol is a potential agent for the prevention of neurons apoptosis by regulating NO and iNOS increase in ERK-mediated neurodegenerative disorders.