Abstract
Scutellarin (Scu), the main bioactive component of Erilgeron breviscapus, protects the brain against ischemic damages. To explore the therapeutic mechanism of Scu, we investigated the impact of Scu on sodium current (I(Na)) of freshly isolated mouse hippocampal CA1 neurons using the whole-cell patch clamp technique. Results showed that Scu inhibited I(Na) in concentration- and holding potential-dependent manners. At 50 μM, Scu markedly shifted the steady state inactivation curve of I (Na) towards a more negative potential, slowed down the recovery of I(Na) from inactivation state, and elicited a frequency-dependent block of I (Na). The shape of the current-voltage (I-V) curve and the steady state activation curve of I(Na) were unaffected by Scu treatment. These findings suggest that Scu is capable of inhibiting I(Na) in neurons through predominantly affecting the inactivated state of I(Na). Inhibition of Na(+) channels provides a novel pharmacological basis for the anti-ischemic application of Scu.
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