CAJ | 학술논문

Objective: α-asarone is a major effective component that can be isolated from Acorus tatarinowii Schott,a Chinese herbal medicine. Clinical investigations have shown that α-asarone has strong sedative and anti-convulsive action in the central nervous system. In recent years, several medicines containing a-asarone were applied in treatment of asthma, bronchitis, expectorant, or epilepsy. However, the underlying cellular mechanism of ct-asarone is still unknown. Here the authors considered EAAC1, the transporter for the excitatory glutamate, as a possible target. Methods: Supercritical CO2 fluid extraction and silica gel column chromatography were used to obtain ct-asarone from the rhizomes of Acorus tatarinowii Schott. Xenopus oocytes with heterologously expressed EAAC 1 were used as a model system. Rate of glutamate uptake was measured by means of isotopic tracer technique. Glutamate-induced current was recorded under two-electrode voltage clamp. 40μg/mL of ct-asarone was used for testing its effect on EAAC1 activity. Results: ct-asarone induced a slight, but still significant stimulation of rate of glutamate uptake by 15%. In contrast, EAACl-mediated current became reduced (by 30% at -100 mV). Since EAAC 1 can operate in transport and also in an ion-channel mode, the result indicates strong inhibition of the channel mode. This inhibition is voltage-dependent becoming larger at more negative potentials. Conclusion: The stimulation of glutamate uptake reduces glutamate concentration in the synaptic cleft and, hence, reduces excitatory synaptic activity. The inhibition on the ion-channel mode stabilizes the membrane potential, and therefore, also contributes to reduced excitatory activity.