Celecoxib is a selective cyclooxygenase-2 (COX-2) inhibitor used in the treatment of osteoarthritis and rheumatoid arthritis with fewer gastrointestinal toxicities compared to traditional non-steroidal anti-inflammatory drugs. Voltage-gated Na + channels in primary sensory neurons play an important role in the pathogenesis of various pain conditions. We examined the effects of celecoxib on tetrodotoxin-sensitive (TTX-S) and tetrodotoxin-resistant (TTX-R) Na + currents in acutely dissociated rat dorsal root ganglion neurons. Celecoxib suppressed both currents in dose- and frequency-dependent manner. The apparent dissociation constants (K d ) for TTX-S and TTX-R Na + currents measured at 0 mV from a holding potential of −80 mV were estimated to be 5.6 and 19.5 μM, respectively. Celecoxib slightly slowed inactivation kinetics of TTX-S Na + current, but made it much faster in TTX-R Na + current. Celecoxib shifted the activation voltage of TTX-S Na + current to a depolarizing direction, but not that of TTX-R Na + current. Celecoxib caused a hyperpolarizing shift of the steady-state inactivation curve in both Na + currents to a great extent. In addition celecoxib reduced the maximal availability of both Na + channels. Thus celecoxib appears to bind to both inactivated and resting Na + channels. Celecoxib slowed the recovery of both Na + channels from inactivation. All these effects combined would suppress the excitability of sensory neurons. Thus, beside COX-2 inhibition, the Na + channel inhibition is considered to contribute to celecoxib analgesia.