Magnolol attenuates inflammatory pain by inhibiting sodium currents in mouse dorsal root ganglion neurons.

Voltage-gated sodium channels are currently recognized as one of the targets of analgesics. Magnolol (Mag), an active component isolated from Magnolia officinalis, has been reported to exhibit analgesic effects. The objective of this study was to investigate whether the analgesic effect of Mag was associated with blocking Na+ channels. Inflammatory pain was induced by the injection of carrageenan into the hind paw of mice. Mag was administered orally. Mechanical hyperanalgesia was evaluated by using von Frey filaments. Na+ currents and neuronal excitability in acutely isolated mouse dorsal root ganglion (DRG) neurons were recorded with the whole-cell patch clamp technique. Results showed that Mag (10 ~ 40 mg/kg) dose-dependently inhibited the paw edema and reduced mechanical pain in the inflammatory animal model. Injection of carrageenan significantly increased the amplitudes of TTX-sensitive and TTX-resistant Na+ currents. Compared with the carrageenan group, Mag inhibited the upregulation of two types of Na+ currents induced by carrageenan in a dose-dependent manner. Mag 40 mg/kg shifted the inactivation curves of two types of Na+ currents to hyperpolarization and returned to normal animal level without changing their activation curves. Mag 40 mg/kg significantly reduced the percentage of cells firing multiple spikes and inhibited the neuronal hyperexcitability induced by carrageenan. Our data suggest that the analgesic effect of Mag may be associated with a decreased neuronal excitability by blocking Na+ current.