Pro-neurogenic effect of β-asarone on RSC96 Schwann cells in vitro

Nerve regeneration is a challenge for the therapy of peripheral nerve injury. beta-Asarone, a major compound extracted from Acorus tatarinowii Schott rhizome, has been traditionally used in China and other parts of Asia for the treatment of common psychiatric diseases. It has been reported to have significant pharmacological effects on the central nervous system. This suggested that beta-asarone may be a promising anti-neuroinflammatory and neuroprotective agent to relieve destruction and accelerate proliferation of Schwann cells after peripheral nerve injury. In this study, we investigated the effects of beta-asarone on RSC96 Schwann cells, a spontaneously immortalized rat Schwann cell line in vitro. RSC96 cells were treated with a range of beta-asarone concentrations ( 090 mu M) for 2, 4, and 6 days. Results showed that beta-asarone at concentrations down to 22.5 mu M were not cytotoxic to RSC96 cells (p<0.05). Concentrations of 5-20 mu M beta-asarone induced a net increase in cell proliferation ( reflected in total DNA) compared to basal medium controls ( p<0.05). beta-Asarone could promote expression of GDNF, BDNF, and CNTF genes (p< 0.05). Furthermore, the viability assay, hematoxylin-eosin, and immunohistochemical staining also showed better performances in beta-asarone groups. As to the doses, 10 mu M beta-asarone showed the best performance. The results indicate that beta-asarone can accelerate proliferation of RSC96 cells in vitro and meanwhile maintain the phenotype, which may provide valuable references for further exploration on peripheral nerve diseases.